tag:theconversation.com,2011:/africa/topics/fruit-flies-3876/articlesFruit flies – The Conversation2023-08-31T13:41:54Ztag:theconversation.com,2011:article/2118472023-08-31T13:41:54Z2023-08-31T13:41:54ZA fruit fly has landed in your wine – is it OK to drink?<figure><img src="https://images.theconversation.com/files/544624/original/file-20230824-25-c2ho4q.jpg?ixlib=rb-1.1.0&rect=18%2C0%2C6039%2C4014&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/fruit-fly-swimming-red-wine-wasnt-2283078405">Anne Webber/Shutterstock</a></span></figcaption></figure><p>You pour a chilled glass of your favourite sauvignon blanc and are about to take a sip when a fruit fly lands in it. The fly is clearly dead. But given what you know about where flies hang out, you wonder if it’s safe to drink.</p>
<p>Despite their salubrious sounding name, fruit flies (<em>Drosophila</em> species),
eat food that is decaying. They inhabit rubbish bins, compost heaps or any place where food is present, including drains. Rotting food is rich in germs, any of which a fly can pick up on their body and transfer to where it next lands.</p>
<p>These <a href="https://www.sciencedirect.com/science/article/pii/S0362028X22084745">bacteria</a> include <em>E coli</em>, <em>Listeria</em>, <em>Shigella</em> and <em>Salmonella</em>, any of which can cause a potentially serious infection in even healthy people. The fruit fly, you realise, may have just deposited potentially lethal microbes in your wine, so you toss it in the sink and pour a fresh glass. </p>
<p>However, the scientific evidence suggests you may have just wasted a good glass of wine. Wine has typically between 8% and 14% ethanol and has a pH of around 4 or 5 – a pH below 7 is considered acidic. </p>
<p>Alcohol is well known to be inhibitory to germs and is one reason wine can be stored for so long. <a href="https://pubmed.ncbi.nlm.nih.gov/9754789/">Several</a> <a href="https://www.mdpi.com/2304-8158/9/7/936">laboratory</a> <a href="https://pubmed.ncbi.nlm.nih.gov/20629891/">studies</a> have also shown that the combined effects of wine alcohol and organic acids, such as malic acid, can prevent the growth of <em>E coli</em> and <em>Salmonella</em>.</p>
<figure class="align-center ">
<img alt="E coli bacteria" src="https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/545266/original/file-20230829-17-jfb8mc.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Wine is known to inhibit the growth of germs, such as E coli.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/escherichia-coli-bacterium-e-gramnegative-rodshaped-1026248248">Kateryna Kon/Shutterstock</a></span>
</figcaption>
</figure>
<p>Whether the germs transmitted by the fruit fly into the wine can cause an infection <a href="https://www.ift.org/news-and-publications/food-technology-magazine/issues/2021/may/columns/food-safety-and-quality-infectious-doses-of-foodborne-illness">depends on</a> the number of bacteria deposited (the “infectious dose”) and how metabolically fit the germs are. The wine the fruit fly entered was also chilled, which some food poisoning bacteria find <a href="https://www.frontiersin.org/articles/10.3389/fmicb.2016.01151/full">shocks their metabolism so profoundly</a> it stops them growing.</p>
<p>As all types of wine (red, white or rosé, whether chilled or room temperature) are naturally antibacterial, germs in wine are <a href="https://pubmed.ncbi.nlm.nih.gov/20629891/">likely to become damaged</a>, which will reduce their infection fitness. This suggests that while the germs deposited into wine by the flies might be present in a dose high enough to cause illness, they are not likely to cause an infection as they are too damaged. So, in all likelihood, the contaminated wine could be drunk without ill effect – whether it was chilled or not.</p>
<h2>Then it has the body to contend with</h2>
<p>And if not damaged directly by the wine, any germs still alive from the fruit fly deposit will encounter the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7684463/pdf/WJG-26-6706.pdf">highly acidic fluids of the human stomach</a>. </p>
<p>Food poisoning germs are highly sensitive to acid, which damages their DNA, and stomach acid can even kill them. In the stomach, germs must also overcome other deadly barriers such as digestive enzymes, entrapping mucus and the ever-watchful immune system defences. Fly-deposited wine germs are <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7553086/pdf/fmicb-11-556140.pdf">unlikely to be able to set up an infection</a>.</p>
<p>Unless you are germ-phobic, I would suggest removing the fly and drinking the wine. If you want the extra protein, you could even swallow the fly.</p>
<p>The fruit fly is unlikely to change the taste of the wine, even if there are several of them. Your digestive system will simply process the fly like any other protein. Salud!</p><img src="https://counter.theconversation.com/content/211847/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Primrose Freestone does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>A microbiologist explains the risks to your health of a fly landing in your chilled glass of sauvignon blanc.Primrose Freestone, Senior Lecturer in Clinical Microbiology, University of LeicesterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2117532023-08-31T09:38:28Z2023-08-31T09:38:28ZBiological clocks: how does our body know that time goes by?<p>In April of this year, Spanish athlete Beatriz Flamini emerged into the light after a 500-day stay in a cave. Her descent underground is <a href="https://www.theguardian.com/world/2023/apr/14/spanish-woman-emerges-after-spending-500-days-living-alone-in-cave">probably the longest undertaken</a> by a long stretch. Flamini says she lost all sense of time on the 65th day. But can she really be sure it was the 65th day? By way of comparison, in 1962 France’s Michel Siffre surfaced from the Scarasson chasm in Italy after spending what he thought was 33 days there. In fact, he spent <a href="https://www.lemonde.fr/a-la-une/article/2005/03/20/michel-siffre-et-son-horloge-de-chair_373377_3208.html">58 days underground</a>.</p>
<h2>The tick of life’s clocks</h2>
<p>How can isolated human beings keep regular track of time, even when they’re disconnected from their surrounding environment? Quite simply, because biological rhythms are at the heart of life, regulating it all the way from the molecular level up to that of the entire body. These include not only our sleep/wake cycles, but also <a href="https://ccsuniversity.ac.in/bridge-library/pdf/Zoology-0505-Circadian-Regulation-of-Metabolism-in-Health-and-Diseases-IV-Unit-3.pdf">body temperature, hormones, metabolism and the cardiovascular system</a>, to name but a few.</p>
<p>And these rhythms have many repercussions, not least in terms of public health. Indeed, a number of diseases are episodic – for example, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733366/#R250">asthma is more severe at night</a>, while cardiovascular accidents are more frequent in the morning. Another example is shift work, which disconnects people from their environment. It may be associated with an increased risk of cancers in workers, prompting the WHO to label it as a <a href="https://doi.org/10.1016/S1470-2045(19)30455-3">probable carcinogen</a>.</p>
<p>Rhythms also impact how we interact with other species. For example, African trypanosomiasis, also called sleeping sickness, is a <a href="https://www.nature.com/articles/s41467-017-02484-2">disorder of our daily rhythm</a> caused by the parasite <em>Trypanosoma brucei</em>, whose <a href="https://www.nature.com/articles/nmicrobiol201732">metabolism is also daily</a> – just like our <a href="https://journals.sagepub.com/doi/10.1177/0748730415577723">immunity</a>.</p>
<h2>Genes: the great clockmakers</h2>
<p>The rotations of the Earth, Moon and Sun generate environmental cycles that have favoured the selection of <a href="https://doi.org/10.1146/annurev.ph.55.030193.000313">biological clocks</a>.</p>
<p>A biological clock is a mechanism internal to organisms that, in the absence of an environmental signal, operates at its own frequency. The regular alternation of day and night has, for example, favoured the evolution of the circadian clock (<em>circa</em>, meaning “approximately”, and <em>diem</em>, “day”).</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Common fruit fly" src="https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/543030/original/file-20230816-29-44orpq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The common fruit fly provides scientists with an excellent model to analyse many developmental and physiological processes, such as the internal clock or the immune system, at the molecular and cellular levels.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/42200412@N03/15022387556/">Géry Parent/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<p>The <a href="https://www.science.org/content/article/timing-everything-us-trio-earns-nobel-work-body-s-biological-clock">circadian clock mechanism was first discovered in the fruit fly</a>, also known as Drosophila, in the 1970s. It is based on feedback loops in the transcription and translation of several genes – gene A promotes the expression of gene B, which in turn inhibits the expression of gene A – creating an oscillation. During the day, light induces the diminution of specific factors of the loop via a photoreceptor called cryptochrome. Interestingly, the key factors in the mechanism essentially only comprise a few genes named <a href="https://doi.org/10.1038/s41580-019-0179-2"><em>period</em>, <em>timeless</em>, <em>clock</em> and <em>cycle</em></a>. However, the fine-tuning and regulation of the clock is based on a complex molecular and neuronal network that ensures its timing and precision.</p>
<figure class="align-center ">
<img alt="Two birds on a branch" src="https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=384&fit=crop&dpr=1 600w, https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=384&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=384&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=483&fit=crop&dpr=1 754w, https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=483&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/543024/original/file-20230816-27-hy87ze.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=483&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">The clock mechanism of great tits has also been studied. The tree on which these tits sit, like plants and fungi, also have biological clocks.</span>
<span class="attribution"><a class="source" href="https://upload.wikimedia.org/wikipedia/commons/8/86/GreatTit002.jpg">Shirley Clarke/Wikipedia</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>There is no single, overarching circadian clock that would organise all of life, as the clock genes vary from species to species. But the principle remains the same: genes whose expression oscillates. Biological rhythms have been described in all the taxa (groups of organisms) studied so far, which comprise cyanobacteria (a type of bacteria that obtain energy via photosynthesis), fungi, plants, and animals, including humans.</p>
<p>In addition, various time givers (<em>zeitgebers</em>) synchronise the organism with its environment: light (the most studied to date), temperature and food, in particular.</p>
<h2>An internal clock synchronised by the environment</h2>
<p>One very concrete implication of this circadian clock concerns <a href="https://www.bbc.com/future/article/20140523-the-science-of-jet-lag">jet lag</a>. This is the deviation of an individual’s internal rhythm from the time of the time zone they are in.</p>
<p>Environmental signals in general, and light in particular, help to re-synchronise the individual: light perceived at the end of the night moves the clock forward, while light perceived at the beginning of the night delays it. Light perceived during the day has no effect. In humans, light is not perceived directly by the molecular clock, but is captured in the retina and then transmitted via the retino-hypothalamic pathway to a central clock, where it modulates the synthesis of clock proteins. The system is not infinitely scalable, however: it takes the human body approximately one day to adapt to a one-hour time difference.</p>
<p>With <em>Homo sapiens</em>‘ intrinsic circadian period spanning <a href="https://pubmed.ncbi.nlm.nih.gov/18419318/">an average 24.2 hours</a>, it is easier for us to travel west and lengthen our days than to travel east and shorten them. This is also why athletes and researchers who isolate themselves in the depths of the Earth end up being out of sync with time on the surface, and ultimately perceive fewer days than 24-hour solar days.</p>
<h2>Other times, other clocks</h2>
<p>The circadian clock is not the only clock mechanism that exists in nature. Many biological processes are <a href="http://dx.doi.org/10.1098/rspb.2013.0016">seasonal</a>, such as the migration of a host of birds and insects, the reproduction and hibernation of many animal species and the flowering of plants. This seasonality is generally dictated by several factors, including by what is known as a <a href="http://dx.doi.org/10.1098/rstb.2016.0252">circannual clock</a> in the case of many species. The mechanism of this clock has not yet been determined.</p>
<p>The clock mechanisms in marine species are also unknown, partly because of the oceans’ <a href="https://doi.org/10.1146/annurev-marine-030422-113038">complex temporal structure</a>. Marine organisms are exposed to the solar cycle of alternating day and night, which is superimposed on a series of lunar cycles, the most prominent of which is the tidal cycle (with a period of 12.4 hours or 24.8 hours). The semi-lunar and lunar cycles (14.8 days/29.5 days), linked to the phases of the moon, also strongly modulate the marine environment, via light and tides. The seasons also affect these ecosystems.</p>
<figure class="align-center ">
<img alt="Victor6000 submersible during a campaign" src="https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=301&fit=crop&dpr=1 600w, https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=301&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=301&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=378&fit=crop&dpr=1 754w, https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=378&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/543025/original/file-20230816-15-vt881v.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=378&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Sampling the deep ocean is always a technical challenge: these deep seas are tricky to access, plunged into darkness, and subject to very high pressures. To explore them requires a submersible, in this case the Victor6000.</span>
<span class="attribution"><a class="source" href="https://www.nature.com/articles/s41467-020-17284-4/figures/1">JY Collet//Ifremer</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<figure class="align-center ">
<img alt="Sampling and preservation of samples using the ROV" src="https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=356&fit=crop&dpr=1 600w, https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=356&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=356&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=448&fit=crop&dpr=1 754w, https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=448&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/543026/original/file-20230816-19-rfkqow.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=448&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">To study the biological rhythms of hydrothermal mussels under realistic conditions, they were sampled using the ROV and then preserved directly on the ocean floor, at a depth of 1,700 metres, in a solution that ‘froze’ their biological time. These samples were taken under red light and very precisely, every 2 hours and 4 minutes for a total of 24 hours and 48 minutes.</span>
<span class="attribution"><a class="source" href="https://www.nature.com/articles/s41467-020-17284-4/figures/1">Ifremer/Nature Communications</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>While complex, the temporal structure of marine environments is predictable, and biological rhythms linked to all these cycles have been described in marine species. For example, many corals <a href="https://www.barrierreef.org/news/explainers/what-is-coral-spawning-great-barrier-reef">synchronise their reproduction</a>, laying eggs once a year over a very short period of time. Some marine worms swarm precisely <a href="https://www.pnas.org/doi/full/10.1073/pnas.2115725119">once a month</a>, in the darkest hours of the night, to initiate their reproductive dance before spawning and dying.</p>
<p>Interestingly, in 2020, our team of scientists revealed that biological rhythms are not limited to the coastal environment. We indeed showed <a href="https://doi.org/10.1038/s41467-020-17284-4">rhythms in behaviour and gene expression at a depth of 1,700 metres</a>, in a mussel living in the hydrothermal vents of the mid-Atlantic ridge. Our work underlines that the temporal coordination in physiology is likely critical, even in the most extreme life environments such as the deep ocean.</p><img src="https://counter.theconversation.com/content/211753/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Audrey Mat a reçu des financements de EU Marie Curie Cofund program VIP2</span></em></p>Our bodies are able to perceive time thanks to our internal clocks, which are also used by the other living beings with which we interact.Audrey Mat, Researcher in marine biology and chronobiology, Universität WienLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2120732023-08-27T13:32:44Z2023-08-27T13:32:44ZLearning from failures: Support for scientific research needs to include when things don’t work out<figure><img src="https://images.theconversation.com/files/544660/original/file-20230824-17-fr9wys.jpg?ixlib=rb-1.1.0&rect=10%2C0%2C2378%2C1084&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">A failed experiment led to researchers showing that assumptions about chromosomal behaviour were wrong.</span> <span class="attribution"><span class="source">(Shutterstock)</span></span></figcaption></figure><iframe style="width: 100%; height: 100px; border: none; position: relative; z-index: 1;" allowtransparency="" allow="clipboard-read; clipboard-write" src="https://narrations.ad-auris.com/widget/the-conversation-canada/learning-from-failures-support-for-scientific-research-needs-to-include-when-things-dont-work-out" width="100%" height="400"></iframe>
<p>The cellular processes involved in gene regulation can be unexpectedly complicated. The expression of genes — the when, where and how much of gene activity — underlies all of biology, but is surprisingly poorly understood. </p>
<p>A recent paper published by our research group <a href="https://doi.org/10.1093/genetics/iyac181">generates as many questions as answers</a>, but gives some explanations to possible mechanisms underlying the tangle of gene function. And notably, this published research shouldn’t exist, given the way we generally fund and support scientific research.</p>
<h2>Complexity and genetic regulation</h2>
<p>Biological complexity — the gloriously complicated and convoluted living world around us — is driven by regulation and specificity. </p>
<p>Essentially, every cell in a multicellular organism has the same set of genes known as their genome. What gives cells their unique identity — what makes a skin cell a skin cell and not a muscle cell — is their specific set of genes that are turned on or off. This regulation process is incredibly specific but frustratingly messy, and follows staggeringly tangled webs of rules. </p>
<p>This complexity makes the details of regulation of gene activity one of the great unknowns of modern biology.</p>
<p>In our paper, we explore how chromosomes physically interact and share information, how that sharing substantially modifies gene expression, and how that modification varies drastically between individuals. All three of these points explain some of the complexity in gene expression, but all three have been largely ignored in conventional modelling of gene regulation.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="an x shaped 3-d figure coloured pink and yellow floating among other similar blue shapes" src="https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/544713/original/file-20230825-27-l9lc4q.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Geneticists have long assumed that chromosomes operate independently, but a failed research experiment showed that this was not the case.</span>
<span class="attribution"><span class="source">(Shutterstock)</span></span>
</figcaption>
</figure>
<p>Geneticists have been taught that chromosomes are independent, don’t modify each other’s expression and that gene expression is similar between individuals. Except they aren’t, they do and it isn’t. </p>
<h2>Chromosomal communication</h2>
<p>In a process called <a href="https://doi.org/10.1016/j.cub.2017.08.001">transvection</a>, pairs of chromosomes physically couple, modifying the expression of the genes they contain. We studied the phenomena in fruit flies using an unusual genetic situation we had created by pairing a series of chromosomes with small genetic deletions that inactivate a gene with wild, functional chromosomes. </p>
<p>Other labs have shown that chromosome pairing is part of <a href="https://doi.org/10.1038/s41467-022-31737-y">normal gene regulation</a> and <a href="https://doi.org/10.1016/j.celrep.2022.111910">development</a>. But pairing errors similar to the ones in our study do occur, and they drive at least one type of <a href="https://doi.org/10.1371/journal.pgen.1000176">human cancer</a>. </p>
<p>Transvection is <a href="https://doi.org/10.1016/j.gde.2016.03.002">a widespread process</a> and a powerful example of the hidden complexity of gene regulation. </p>
<p>It is also an example of research we would not have pursued if not for some uncommon direction and mentoring Thomas Merritt, a co-author of this article, received just before starting his own lab.</p>
<p>Our transvection project started as a <a href="https://doi.org/10.1534/genetics.105.048249">failed experiment</a> while Merritt worked in evolutionary geneticist Walt Eanes’s <a href="https://life2.bio.sunysb.edu/ee/eaneslab/">lab at Stony Brook University</a>. As part of a study on metabolic interactions in flies, Merritt had edited a gene to produce a specific level of protein activity. Although the editing worked, there was much higher than expected levels of protein <a href="https://doi.org/10.1534/genetics.111.133231">and gene activity</a>. The experiment had failed. </p>
<p>Fortunately, Eanes explicitly guided researchers under his mentorship to pay attention to the unexpected, including failed experiments, and use them as an opportunity to question assumptions. </p>
<p>Two decades later, <a href="http://www.boscogeneticslab.com/people2">working alongside</a> <a href="https://www.bowdoin.edu/profiles/faculty/jbateman/">other scientists</a>, we’re still <a href="https://www.transvection.org/">finding new complications in genetics</a>.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="a small fly" src="https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/544715/original/file-20230825-17-rz04it.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Studying the genome of Drosophila melanogaster reveals how chromosomes interact with and affect each genetic expression.</span>
<span class="attribution"><span class="source">(Shutterstock)</span></span>
</figcaption>
</figure>
<h2>Failed experiments and scientific assumptions</h2>
<p>That initial experiment had failed — but it had done so for a very interesting reason. That failed experiment, and the series of studies that followed it, showed that what geneticists typically think of as “<a href="https://wyss.harvard.edu/news/light-shed-on-century-old-riddle-of-chromosome-pairing/">independent</a>” chromosomes actually interact with each other through direct physical connections.</p>
<p>That failed experiment illuminated a world of complex regulatory control. Not only do genes have incredibly complex on/off switches, these switches sometimes work across and between chromosomes. </p>
<p>Handled well, these unexpected failures in the lab pushed us to question the assumptions that led to the unexpected result. Here, the failed experiment forced us to rethink the independence of chromosomes. </p>
<p>Our further studies explored how this genetic conversation was dynamic, changed <a href="https://doi.org/10.1534/g3.114.012484">in response to the environment</a> and differed between <a href="https://doi.org/10.1534/genetics.111.133231">individuals</a>.</p>
<h2>Individual variation</h2>
<p>The dynamic gene regulation and individual variation that allows multicellularity is also a central player in disease and individuality. For example, why do some people, but not others, respond to cancer treatments or even fall victim to cancer in the first place? </p>
<p>A better appreciation of individual variation is one of the major advances of our paper. Knowing that the amount of communication between chromosomes varies substantially across individuals and our work begins to shed light on the genes and mechanisms behind that variation. </p>
<p>These are important steps towards a more complete understanding of gene regulation and the misregulation that leads to diseases like <a href="https://openoregon.pressbooks.pub/mhccmajorsbio/chapter/cancer-and-gene-regulation/">cancer</a>. </p>
<h2>Dynamic science</h2>
<p>Science advances when scientists push boundaries and explore, not when we repeat or timidly inch forward. Too often we try to avoid or prevent failure. Funding agencies may also hesitate to fund projects seen as <a href="https://www.science.org/content/article/audacity-part-3-funding-audacious-science">risky</a>. </p>
<p>Science needs a culture that promotes risk and exploring the unexpected.</p>
<p>And while we turn to science to address emerging crises, we are not supporting the necessary scientific development. Think of the increasingly frequent <a href="https://theconversation.com/canadians-are-unprepared-for-natural-hazards-heres-what-we-can-do-about-it-201863">climate disasters</a>, the <a href="https://theconversation.com/the-quest-for-delicious-decaf-coffee-could-change-the-appetite-for-gmos-153032">challenges of feeding an exploding global population</a>, <a href="https://doi.org/10.1038/s41586-019-1717-y">the ongoing global pandemic</a> and <a href="https://www.nytimes.com/2023/06/16/opinion/cancer-treatment-disparities.html">cancer</a>.</p>
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Read more:
<a href="https://theconversation.com/doctors-are-drowning-in-a-tsunami-of-liver-disease-and-cancer-98061">Doctors are drowning in a tsunami of liver disease and cancer</a>
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</em>
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<p>All of these issues will require novel solutions and dynamic approaches that scientific funding agencies should <a href="https://www.forbes.com/sites/drdonlincoln/2021/06/28/why-you-should-care-about-federally-funded-science/">acknowledge and support</a>.</p>
<p>Breakthroughs in understanding require dynamic science and scientists who are supported to explore, ask unusual questions and, occasionally, fail in the lab. Sometimes the most important results from an experiment are the questions it forces us to ask.</p><img src="https://counter.theconversation.com/content/212073/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Thomas Merritt receives funding from the Natural Sciences and Engineering Research Council of Canada.</span></em></p><p class="fine-print"><em><span>Teresa Rzezniczak does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>A failed experiment led the researchers to question their assumptions and realize that, contrary to popular belief, chromosomes interact with and affect genetic expression.Thomas Merritt, Professor, Chemistry and Biochemistry, Laurentian UniversityTeresa Rzezniczak, PhD Candidate, Biomolecular Sciences, Laurentian UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2072832023-06-13T18:25:16Z2023-06-13T18:25:16ZSeeing dead fruit flies is bad for the health of fruit flies – and neuroscientists have identified the exact brain cells responsible<figure><img src="https://images.theconversation.com/files/531186/original/file-20230609-5996-byp5nm.png?ixlib=rb-1.1.0&rect=0%2C0%2C2510%2C1995&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">For _Drosophila melanogaster_, their senses have a significant effect on how quickly they age.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/drosophila-melanogaster-royalty-free-image/108149276">nico_blue/E+ via Getty Images</a></span></figcaption></figure><p><a href="https://www.ncbi.nlm.nih.gov/books/NBK10041/">All living organisms age</a>. People have long sought ways to slow, halt or reverse this process, which is commonly associated with declining mental and physical health. One area researchers are probing is the role that sensory perception – such as sight, smell, sound, taste and touch – plays on health and life span. </p>
<p>While you may typically think of your senses as what you use to gather information about your surroundings, recent work has demonstrated that environmental cues themselves can <a href="https://doi.org/10.1016/j.tem.2016.03.007">affect physiology and aging</a>. Your body regulates itself to match the conditions it finds itself in. The <a href="https://doi.org/10.1146/annurev-physiol-021119-034440">nervous system is poised as a central player</a> in mediating the effects of sensory perception. It stores and integrates incoming information from the environment and interprets and disseminates information across different tissues. </p>
<p>I have used fruit flies, specifically <em>Drosophila melanogaster</em>, for more than 15 years to better understand how <a href="https://www.researchgate.net/profile/Christi-Gendron">sensory perception affects aging</a>. Recently my work has focused on the role the brain plays in aging, looking at how death perception, or when fruit flies perceive other dead fruit flies, affects their life span. My colleagues and I have shown that when fruit flies see, and to a lesser extent smell, an excess of dead flies in their environment, they <a href="https://doi.org/10.1038/s41467-019-10285-y">avoid other flies and undergo significant physiological changes</a>, including rapid decreases in stored fat, decreased resistence to starvation and shortened life span. While it is currently unknown whether these changes are evolutionarily advantageous, we speculate that it could be, because of the stressful environment that the living flies find themselves in.</p>
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<iframe width="440" height="260" src="https://www.youtube.com/embed/MYzEHuaL3e8?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Fruit flies are among the most common model organisms in research.</span></figcaption>
</figure>
<p>In our newly published research, my colleagues and I identified the <a href="http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002149">neural circuits and signaling processes</a> behind the physiological effects, including rapid aging, that occur when <em>Drosophila</em> encounter their dead. Because other animals also experience physiological effects in the presence of their dead, identifying how this process works in fruit flies could shed light on how it operates in other species, including in people.</p>
<h2>Neuroscience of death perception</h2>
<p>Using genetic tools that detect which neurons are likely activated when live flies are exposed to dead flies, we identified a handful of neurons in the <em>Drosophila</em> brain called R2/R4 neurons that <a href="http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002149">act as a rheostat for aging</a>. These neurons are the center of sensory information processing and motor coordination in fruit fly brains. Inhibiting or activating them changed the aging rate of the flies, suggesting that these neurons alter fly life span in response to perceiving dead flies.</p>
<p>Next, we wanted to identify which molecules produced by R2/R4 neurons were responsible for spurring aging after flies witnessed other dead flies. Since components of a signaling pathway involved in glucose regulation have <a href="https://doi.org/10.1038/nature08980">long been associated with aging</a>, we focused on a protein called Foxo that is associated with the pathway.</p>
<p>We discovered that flies without Foxo had similar life spans whether or not there were dead flies present. We saw the same result when we decreased the amount of Foxo in R2/R4 neurons. These findings suggest that <a href="http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002149">Foxo in R2/R4 neurons</a> plays a key role in changing the life span of living flies.</p>
<p>We also discovered that other components of the signaling pathway involved in glucose regulation, called <a href="http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002149"><em>Drosophila</em> insulin-like peptides, or dilps</a>, mediate the effect of death perception on life span. Because these molecules appeared after changes in R2/R4 neuron activity, this suggests that they do not directly affect Foxo in these neurons. They likely work on other tissues.</p>
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<figcaption><span class="caption">Ring neurons like R2/R4 are involved in fruit fly sensory processing and motor coordination.</span></figcaption>
</figure>
<h2>Evolution of sensory perception effects on aging</h2>
<p>There are many examples of how sensory perception affects aging in animals, suggesting that it is a phenomenon that occurs across species. </p>
<p>For example, manipulating specific subsets of sensory neurons in the worm <a href="https://doi.org/10.1016/s0896-6273(03)00816-x"><em>Caenorhabditis elegans</em></a> can either shorten or extend its life span. Genetically manipulating fruit flies to <a href="https://doi.org/10.1126/science.1136610">lose their sense of smell</a> makes them live longer. Furthermore, environmental cues that indicate the presence of <a href="https://doi.org/10.1093/gerona/glv039">food</a>, <a href="https://doi.org/10.1073/pnas.1315461111">water</a>, <a href="https://doi.org/10.1371/journal.pbio.1000356">danger</a> and <a href="https://doi.org/10.1126/science.1243339">potential mates</a> all significantly influence physiology and longevity. </p>
<p>Manipulating the sensory system can affect aging even in mammals. For example, <a href="https://doi.org/10.1016/j.cell.2014.03.051">losing a specific pain receptor</a> can significantly extend the life span of mice.</p>
<p>The effects of seeing dead fruit flies on the physiology of fruit flies resemble changes seen in other species. For instance, <a href="https://doi.org/10.1073/pnas.0901270106">social insects</a> like ants and honeybees carry their dead away from the colony in a behavior called necrophoresis. <a href="https://doi.org/10.1098/rspb.2005.3378">Nonhuman primates</a> also experience increased glucocorticoid levels when a relative dies. This suggests that the processes that mediate these changes have similarities across species. My research team has previously shown that the effects of death perception in <em>Drosophila</em> involved chemical compounds and neural signaling that have been <a href="https://doi.org/10.1038/s41467-019-10285-y">conserved throughout evolution</a>.</p>
<p>The specific cues that lead to changes in the life spans of worms, flies and mice are likely species-specific. But the fact that they are all affected by changes in sensory input suggests that the molecular mechanisms driving age-related changes may be shared by all, including people.</p>
<p>Altogether, our work provides insight into the neural underpinnings of how the senses affect aging. While translating these findings to humans is clearly speculative, we hope that more research can eventually help researchers better understand the physiological and psychological effects of people who routinely witness death, such as soldiers and first responders.</p><img src="https://counter.theconversation.com/content/207283/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Christi Gendron does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>When fruit flies see other dead fruit flies, their life spans are cut short. Other species also undergo analogous physiological changes when seeing their dead.Christi Gendron, Research Assistant Professor of Molecular and Integrative Physiology, University of MichiganLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1714562021-11-10T19:11:16Z2021-11-10T19:11:16ZGenetic GPS system of animal development explains why limbs grow from torsos and not heads<figure><img src="https://images.theconversation.com/files/431177/original/file-20211109-25-10ge7mq.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C703%2C496&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">New research in fruit flies elucidates how the genes that direct animal body shape work.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/close-up-of-insect-head-royalty-free-image/707582343">Vaclav Hykes/EyeEm via Getty Images</a></span></figcaption></figure><p>Why do human look like humans, rather than like chimps? Although we <a href="https://www.science.org/content/article/bonobos-join-chimps-closest-human-relatives">share 99% of our DNA</a> with chimps, our faces and bodies look quite different from each other.</p>
<p>While human body shape and appearance have clearly changed during the course of evolution, some of the genes that control the defining characteristics of different species surprisingly have not. As a <a href="https://biology.ucsd.edu/research/faculty/ebier">biologist studying evolution and development</a>, I have devoted many years to pondering how genes actually make people and other animals look the way they do. </p>
<p><a href="https://doi.org/10.1126/sciadv.abk1003">New research</a> from my lab on how these genes work has shed some light on how genes that have remained unchanged for hundreds of thousands of years can still alter the appearance of different species as they evolve.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1195486216843513856"}"></div></p>
<h2>Heads versus tails</h2>
<p>In biology, a <a href="https://doi.org/10.1242/dev.039651">body plan</a> describes how an animal’s body is organized from head to toe – or tail. All animals with <a href="https://courses.lumenlearning.com/boundless-biology/chapter/features-used-to-classify-animals/">bilateral symmetry</a>, meaning their left and right sides are mirror images, share similar body plans. For example, the head forms at the anterior end, limbs form in the mid-body, and the tail forms at the posterior end.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram of three body plan symmetries of animals (asymmetrical, radial and bilateral)." src="https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=247&fit=crop&dpr=1 600w, https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=247&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=247&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=311&fit=crop&dpr=1 754w, https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=311&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/431128/original/file-20211109-15-z4had2.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=311&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Animals in the same species usually share the same symmetry. Humans and goats have bilateral symmetry, meaning they can be divided into halves that are mirror images of each other.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Figure_33_01_01.jpg">CNX OpenStax/Wikimedia Commons</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
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</figure>
<p><a href="https://doi.org/10.1038/nrg1726">Hox genes</a> play an important role in setting up this body plan. This group of genes is a subset of genes involved in anatomical development called <a href="https://doi.org/10.1016/0092-8674(92)90471-n">homeobox genes</a>. They act like a genetic GPS system, determining what each body segment will turn into during development. They ensure that your limbs grow from your torso instead of from your head by controlling other genes that instruct the formation of specific body parts. </p>
<p>All animals have Hox genes and express them in similar body regions. Furthermore, these genes haven’t changed throughout evolutionary history. How can these genes remain so stable over such vast evolutionary time spans, yet play such pivotal roles in animal development?</p>
<h2>Blast from the past</h2>
<p>In 1990, molecular biologist <a href="https://biology.ucsd.edu/research/faculty/wmcginnis">William McGinnis</a> and his research team wondered whether the Hox genes from one species might function similarly in another species. After all, these genes are active in similar body regions in animals ranging from fruit flies to humans and mice.</p>
<p>This was a bold idea. As an analogy, consider cars: Most car parts typically are not interchangeable between different makes. The <a href="https://www.loc.gov/everyday-mysteries/item/who-invented-the-automobile/">first automobile</a> was only invented around 100 years ago. Compare that to flies and mammals, whose <a href="https://doi.org/10.1534/genetics.114.171785">last common ancestor</a> lived over 500 million years ago. It was virtually unthinkable that swapping genes from different species that diverged from each other over such a vast period of time could work.</p>
<p>Nonetheless, McGinnis and his team went ahead with their experiment and inserted mouse or human Hox genes into fruit flies. They then activated the genes in the wrong corresponding areas of the body – for instance, placing the Hox gene that tells a human leg where to develop at the very front of a fruit fly’s head. A misplaced body part would indicate that the mouse or human Hox genes were functioning like the fruit fly’s own genes would have.</p>
<p>Remarkably, both <a href="https://doi.org/10.1016/0092-8674(90)90499-5">mouse</a> and <a href="https://doi.org/10.1016/0092-8674(90)90500-E">human</a> Hox genes transformed the fruit fly antennae into legs. This meant that the positional information provided by the human and mouse genes was still recognized in the fly, millions of years later.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1195489028549660678"}"></div></p>
<h2>How do Hox genes really work?</h2>
<p>The next big question, then, was how exactly do these Hox genes determine the identities of different body regions?</p>
<p>There have been two schools of thought on how Hox genes work. The first, called the <a href="https://doi.org/10.1038/nrg2417">instructive hypothesis</a>, proposes that these shape-controlling genes function as “master” regulatory genes that supply the body instructions on how to develop different body parts. </p>
<p>The second, proposed by McGinnis, hypothesizes that Hox genes instead provide a <a href="https://doi.org/10.1038/nrg1726">positional code</a> that marks particular locations in the body. Genes can use these codes to produce specific body structures at those locations. Over the course of evolution, specific body parts come under the control of a specific Hox gene in a way that would best maximize the organism’s survival. This is why flies develop antennae rather than legs on their heads, and humans have collar bones below instead of above their necks.</p>
<p>In a <a href="https://doi.org/10.1126/sciadv.abk1003">recent study</a> published in the journal Science Advances, a mentee of McGinnis and myself, <a href="https://scholar.google.com/citations?user=aQAMm3kAAAAJ&hl=en">Ankush Auradkar</a>, puts these hypotheses to the test on fruit flies.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram showing Drosophola Hox genes and their corresponding body parts." src="https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=420&fit=crop&dpr=1 600w, https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=420&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=420&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=527&fit=crop&dpr=1 754w, https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=527&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/431136/original/file-20211109-13-xlwasg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=527&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Each Hox gene is linked to a specific body part. The proboscipedia gene, or pb, for instance, directs formation of a fruit fly’s mouthparts.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Hox-genes-drosophila.jpg">Antonio Quesada Díaz/Wikimedia Commons</a></span>
</figcaption>
</figure>
<p>Auradkar focused on a fruit fly Hox gene called proboscipedia (<em>pb</em>), which directs the formation of the fly’s mouthparts. He used <a href="https://medlineplus.gov/genetics/understanding/genomicresearch/genomeediting/">CRISPR-based genome editing</a> to replace the <em>pb</em> gene from the common laboratory variety of fruit fly, <em>Drosophila melanogaster</em>, or <em>D. mel</em> for short, with its Hawaiian cousin, <em>Drosophila mimica</em> or <em>D. mim</em>. If the instructive hypothesis were correct, <em>D. mel</em> would form <em>D. mim</em>‘s grill-like mouthparts. Conversely, if McGinnis’ hypothesis were correct, <em>D. mel</em>‘s mouthparts should stay the same.</p>
<p>As McGinnis predicted, the flies with the <em>D. mim</em> genes did not develop <em>D. mim</em>’s grill-like features. There was one feature of <em>D. mim</em>’s, however, that did sneak through: Sensory organs called maxillary palps that usually stick out from the face for <em>D. mel</em> were instead aligned parallel to the mouth. This showed that the <em>pb</em> gene provided both a marker for where the mouth should form as well as instructions on how to form it. Though the main outcome favored McGinnis’ theory, both hypotheses were largely correct.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Side-by-side comparison of the mouthparts of the _D. mel_ and _D. mim_ fruit fly species." src="https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=212&fit=crop&dpr=1 600w, https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=212&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=212&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=266&fit=crop&dpr=1 754w, https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=266&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/431137/original/file-20211109-19-1g7uz6.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=266&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption"><em>D. mel</em> and <em>D. mim</em> have mouthparts, colored tan here, that look very different from each other.</span>
<span class="attribution"><a class="source" href="https://doi.org/10.1126/sciadv.abk1003">Ankush Auradkar</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span>
</figcaption>
</figure>
<p>Auradkar also wondered how the <em>pb</em> gene determined the orientation of the maxillary palps. It could have done this by changing the protein it encodes, which carries out the instructions given by the gene. Or it could have changed how it controls other genes, acting like a light switch that determines when and where genes are turned on. Through more testing, he found that this <em>D. mim</em> feature resulted from changing how strongly the <em>pb</em> gene turns on in regions that form the palps, as opposed to changes in the protein itself. This finding highlights once again the remarkable preservation of Hox protein function over evolution – the genetic hardware worked as well in one species as the other. </p>
<p>Auradkar also found that Hox genes engage in an evolutionary tug-of-war with each other. One Hox gene may become more dominant than another and determine what features will ultimately form in a species.</p>
<p>These experiments showed that even subtle changes in how Hox genes interact with each other can have significant consequences for an organism’s body shape.</p>
<h2>Hox genes and human health</h2>
<p>What do these fly studies mean for people? </p>
<p>First, they provide a window into how the body plans of different species change over the course of evolution. Understanding how Hox genes can manipulate animal development to promote their survival could elucidate why animals look the way they do. Similar mechanisms could explain why humans no longer look like chimps.</p>
<p>Second, these insights may lead to a better understanding of how <a href="https://www.who.int/news-room/fact-sheets/detail/congenital-anomalies">congenital birth defects</a> arise in people. Changes, or mutations, that disrupt the normal functioning of Hox genes could result in conditions like cleft lip or congenital heart disease. New therapies on the horizon using CRISPR-based genome editing could be used to treat these often debilitating conditions, including <a href="https://doi.org/10.1126/science.aau1549">muscular dystrophy</a>.</p>
<p>[<em>Get the best of The Conversation, every weekend.</em> <a href="https://theconversation.com/us/newsletters/weekly-highlights-61?utm_source=TCUS&utm_medium=inline-link&utm_campaign=newsletter-text&utm_content=weeklybest">Sign up for our weekly newsletter</a>.]</p><img src="https://counter.theconversation.com/content/171456/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ethan Bier has equity interest in two companies he co-founded: Synbal Inc. and Agragene, Inc., which may potentially benefit from the research results. He also serves on Synbal's board of directors and the scientific advisory board for both companies.</span></em></p>Hox genes make sure all your body parts grow in the right place. Understanding how they work can reveal the process of evolution and lead to potential treatments for congenital birth defects.Ethan Bier, Professor of Cell and Developmental Biology, University of California, San DiegoLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1653422021-08-19T10:43:09Z2021-08-19T10:43:09ZThe biological switch that could turn neuroplasticity on and off in the brain – podcast<figure><img src="https://images.theconversation.com/files/416766/original/file-20210818-27-1r7iutw.jpg?ixlib=rb-1.1.0&rect=161%2C224%2C5757%2C3592&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Astrocytes: these cells could be part of the key to unlocking the mystery of how brains change their structure. </span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/astrocytes-brain-glial-cells-3d-illustration-1412136197">Kateryna Kon/Shutterstock</a></span></figcaption></figure><p><em><a href="https://theconversation.com/uk/topics/the-conversation-weekly-98901">The Conversation Weekly</a> podcast is taking a short break in August. For the next few weeks we’re bringing you extended versions of some our favourite interviews from the past few months.</em></p>
<p>This week, how researchers discovered a biological switch that could turn neuroplasticity on and off in the brain. What might that mean?</p>
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<p><iframe id="tc-infographic-561" class="tc-infographic" height="100" src="https://cdn.theconversation.com/infographics/561/4fbbd099d631750693d02bac632430b71b37cd5f/site/index.html" width="100%" style="border: none" frameborder="0"></iframe></p>
<p>Neuroplasticity is the ability of neurons in the brain to change their structure. It’s what allows the brains of young animals to change more easily than brains of old animals – and it’s one of the reasons why it’s easier for children to learn languages than adults. </p>
<p>There’s still a lot researchers don’t know about this critical function of the brain. But we do know that many diseases are caused by too little or too much neuroplasticity, and so being able to dial it up or down could have some really important medical benefits. </p>
<p>Sarah Ackerman, a postdoctoral fellow at the Institute of Neuroscience and Howard Hughes Medical Institute at the University of Oregon, studies fruit flies and the mechanisms that turn neuroplasticity on and off in their brains. She talked to us about her team’s <a href="https://www.nature.com/articles/s41586-021-03441-2">new research findings</a> into how these changes are controlled by a type of brain cell called astrocytes. The goal is to help fight diseases, but this work could also potentially unlock the superpowered learning that comes with a malleable brain. </p>
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Read more:
<a href="https://theconversation.com/astrocyte-cells-in-the-fruit-fly-brain-are-an-on-off-switch-that-controls-when-neurons-can-change-and-grow-158601">Astrocyte cells in the fruit fly brain are an on-off switch that controls when neurons can change and grow</a>
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<p>This episode of The Conversation Weekly features an extended version of an interview <a href="https://theconversation.com/scotland-why-may-election-is-crucial-for-independence-movement-and-the-uk-podcast-159883">first published on April 29</a>. The episode was produced by Mend Mariwany and Gemma Ware, with sound design by Eloise Stevens. Our theme music is by Neeta Sarl. You can find us on Twitter <a href="https://twitter.com/TC_Audio">@TC_Audio</a>, on Instagram at <a href="https://www.instagram.com/theconversationdotcom/?hl=en">theconversationdotcom</a>. or via email on podcast@theconversation.com. You can also sign up to <a href="https://theconversation.com/newsletter?utm_campaign=PodcastTCWeekly&utm_content=newsletter&utm_source=podcast">The Conversation’s free daily email here</a>.</p>
<p><em>You can listen to The Conversation Weekly via any of the apps listed above, download it directly via our <a href="https://feeds.acast.com/public/shows/60087127b9687759d637bade">RSS feed</a>, or find out how else to <a href="https://theconversation.com/how-to-listen-to-the-conversations-podcasts-154131">listen here</a>.</em></p><img src="https://counter.theconversation.com/content/165342/count.gif" alt="The Conversation" width="1" height="1" />
From the archive: new research helps unpick clues about the brain’s ability to change its structure. Listen to The Conversation Weekly podcast.Gemma Ware, Head of AudioDaniel Merino, Associate Breaking News Editor and Co-Host of The Conversation Weekly PodcastLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1586012021-04-12T12:28:55Z2021-04-12T12:28:55ZAstrocyte cells in the fruit fly brain are an on-off switch that controls when neurons can change and grow<figure><img src="https://images.theconversation.com/files/394301/original/file-20210409-17-yp356o.jpg?ixlib=rb-1.1.0&rect=14%2C44%2C1060%2C668&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The colors in this microscope photo of a fruit fly brain show different types of neurons and the cells that surround them in the brain.</span> <span class="attribution"><a class="source" href="https://www.doelab.org/">Sarah DeGenova Ackerman</a>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span></figcaption></figure><p><em>The <a href="https://theconversation.com/us/topics/research-brief-83231">Research Brief</a> is a short take about interesting academic work.</em></p>
<h2>The big idea</h2>
<p>Neuroplasticity – the ability of neurons to <a href="https://doi.org/10.1098/rstb.2016.0158">change their structure and function in response to experiences</a> – can be turned off and on by the cells that surround neurons in the brain, <a href="https://doi.org/10.1038/s41586-021-03441-2">according to a new study</a> on fruit flies that I co-authored.</p>
<p>As fruit fly larvae age, their neurons shift from a highly adaptable state to a stable state and lose their ability to change. During this process, support cells in the brain – called astrocytes – <a href="https://doi.org/10.1016/j.neuron.2017.09.056">envelop the parts of the neurons</a> that send and receive electrical information. When my team removed the astrocytes, the neurons in the fruit fly larvae remained plastic longer, hinting that somehow astrocytes suppress a neuron’s ability to change. We then discovered two specific proteins that regulate neuroplasticity.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Fruit flies on a table." src="https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=388&fit=crop&dpr=1 600w, https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=388&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=388&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=488&fit=crop&dpr=1 754w, https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=488&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/394336/original/file-20210409-17-346mnx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=488&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">As fruit flies develop, special cells surround their neurons and seem to halt neuroplasticity.</span>
<span class="attribution"><span class="source">Sarah DeGenova Ackerman</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<h2>Why it matters</h2>
<p>The human brain is made up of billions of neurons that form complex connections with one another. Flexibility at these connections is a <a href="https://doi.org/10.1073/pnas.1820836117">major driver of learning and memory</a>, but things can go wrong if it isn’t tightly regulated. For example, in people, too much plasticity at the wrong time is linked to brain disorders such as <a href="https://doi.org/10.1016/j.cub.2015.09.040">epilepsy</a> and <a href="https://doi.org/10.1016/S0896-6273(00)81109-5">Alzheimer’s disease</a>. Additionally, reduced levels of the two neuroplasticity-controlling proteins we identified are linked to increased susceptibility to <a href="https://doi.org/10.3389/fncel.2018.00470">autism</a> and <a href="https://doi.org/10.1038/s41380-020-00944-8">schizophrenia</a>.</p>
<p>Similarly, in our fruit flies, removing the cellular brakes on plasticity permanently impaired their crawling behavior. While fruit flies are of course different from humans, their brains work in very similar ways to the human brain and can offer valuable insight.</p>
<p>One obvious benefit of discovering the effect of these proteins is the potential to treat some neurological diseases. But since a neuron’s flexibility is closely tied to learning and memory, in theory, researchers might be able to <a href="https://doi.org/10.1111/nyas.12682">boost plasticity</a> in a controlled way to <a href="https://doi.org/10.1098/rstb.2013.0288">enhance cognition in adults</a>. This could, for example, allow people to more easily learn a new language or musical instrument. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A colorful microscope image of a developing fruit fly brain." src="https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=342&fit=crop&dpr=1 600w, https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=342&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=342&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=430&fit=crop&dpr=1 754w, https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=430&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/394317/original/file-20210409-13-1a039sz.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=430&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">In this image showing a developing fruit fly brain on the right and the attached nerve cord on the left, the astrocytes are labeled in different colors showing their wide distribution among neurons.</span>
<span class="attribution"><span class="source">Sarah DeGenova Ackerman</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
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<h2>How we did the work</h2>
<p><a href="https://scholar.google.com/citations?user=-sssMIEAAAAJ&hl=en&oi=sra">My colleagues and I</a> focused our experiments on a specific type of neurons called motor neurons. These control movements like <a href="https://doi.org/10.1186/s13064-018-0103-z">crawling</a> and <a href="https://doi.org/10.1002/cne.903400311">flying</a> in fruit flies. To figure out how astrocytes controlled neuroplasticity, we used genetic tools to turn off specific proteins in the astrocytes one by one and then measured the effect on motor neuron structure. We found that astrocytes and motor neurons communicate with one another using a specific pair of proteins called neuroligins and neurexins. These proteins essentially function as an off button for <a href="https://doi.org/10.1038/s41586-021-03441-2">motor neuron plasticity</a>.</p>
<h2>What still isn’t known</h2>
<p>My team discovered that two proteins can control neuroplasticity, but we don’t know how these cues from astrocytes cause neurons to lose their ability to change.</p>
<p>Additionally, researchers still know very little about why neuroplasticity is so strong in younger animals and <a href="https://doi.org/10.1073/pnas.1820836117">relatively weak in adulthood</a>. In our study, we showed that prolonging plasticity beyond development can sometimes be <a href="https://doi.org/10.1038/s41586-021-03441-2">harmful to behavior</a>, but we don’t yet know why that is, either. </p>
<p>[<em>Understand new developments in science, health and technology, each week.</em> <a href="https://theconversation.com/us/newsletters/science-editors-picks-71/?utm_source=TCUS&utm_medium=inline-link&utm_campaign=newsletter-text&utm_content=science-understand">Subscribe to The Conversation’s science newsletter</a>.]</p>
<h2>What’s next</h2>
<p>I want to explore why longer periods of neuroplasticity can be harmful. Fruit flies are great study organisms for this research because it is very easy to <a href="https://doi.org/10.1038/nmeth.1567">modify the neural connections in their brains</a>. In my team’s next project, we hope to determine how changes in neuroplasticity during development can lead to long–term changes in behavior.</p>
<p>There is so much more work to be done, but our research is a first step toward treatments that use astrocytes to influence how neurons change in the mature brain. If researchers can understand the basic mechanisms that control neuroplasticity, they will be one step closer to developing therapies to treat a variety of neurological disorders.</p>
<p><em>To learn more about Sarah DeGenova Ackerman’s research on fruit flies and neuroplasticity, tune in to this episode of The Conversation Weekly podcast.</em></p>
<iframe src="https://embed.acast.com/60087127b9687759d637bade/60899b812984c378fd29a86a?cover=true&ga=false" frameborder="0" allow="autoplay" width="100%" height="110"></iframe><img src="https://counter.theconversation.com/content/158601/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sarah DeGenova Ackerman receives funding from the NIH/NINDS. Sarah DeGenova Ackerman is a Milton Safenowitz postdoctoral fellow of the ALS Association.</span></em></p>Adaptable neurons are tied to learning and memory but also to neurological disorders. By studying fruit flies, researchers found a mechanism that controls neuroplasticity.Sarah DeGenova Ackerman, Postdoctoral Fellow, UO Institute of Neuroscience and Howard Hughes Medical Institute, University of OregonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1536732021-01-21T14:32:20Z2021-01-21T14:32:20ZPollinators: neonicotinoid pesticides stop bees and flies from getting a good night’s sleep<figure><img src="https://images.theconversation.com/files/379975/original/file-20210121-17-1pzg39p.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C3543%2C2386&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Sleeping on the job?</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/focus-stacking-bufftailed-bumblebee-dumbledor-dumbledore-636775153">Maciej Olszewski/Shutterstock</a></span></figcaption></figure><p>Neonicotinoids, the most commonly used pesticides in the world, were <a href="https://www.theguardian.com/environment/2018/apr/27/eu-agrees-total-ban-on-bee-harming-pesticides">banned in the EU</a> in 2018. More than <a href="https://petition.parliament.uk/archived/petitions/104796">99,000 people</a> petitioned the UK government to support the ban amid a wealth of scientific evidence linking this group of chemicals to poor health in bees, from the reduced production of <a href="https://science.sciencemag.org/content/336/6079/351">bumblebee queens</a> to <a href="https://royalsocietypublishing.org/doi/10.1098/rspb.2016.0506">slashed sperm counts</a> among male honeybees.</p>
<p>The UK government had <a href="https://www.theguardian.com/environment/2017/nov/09/the-evidence-points-in-one-direction-we-must-ban-neonicotinoids">pledged</a> to keep the EU’s restrictions post-Brexit, but recently <a href="https://www.gov.uk/government/publications/neonicotinoid-product-as-seed-treatment-for-sugar-beet-emergency-authorisation-application/statement-on-the-decision-to-issue-with-strict-conditions-emergency-authorisation-to-use-a-product-containing-a-neonicotinoid-to-treat-sugar-beet">granted a special exemption</a> to allow farmers to use the neonicotinoid thiamethoxam on sugarbeet throughout 2021, and possibly until 2023.</p>
<p>If this signals the government’s intention to roll back regulations on agricultural chemicals now that the UK has left the EU, the consequences for pollinating insects could be dire. Research into the effects of these pesticides on pollinators is still ongoing, but new harmful effects are discovered all the time.</p>
<figure class="align-center ">
<img alt="A tractor sprays chemicals onto a vegetable field at dusk." src="https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/379966/original/file-20210121-19-gkw885.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Neonicotinoids are sprayed onto farm fields to control pests such as aphids and grubs.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/tractor-spraying-pesticides-on-vegetable-field-664124608">Fotokostic/Shutterstock</a></span>
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<p>In <a href="https://www.nature.com/articles/s41598-021-81548-2">a new study</a>, my colleagues and I have uncovered the most recent example. We looked into the effect of these pesticides on the body clock and sleep of flies and bumblebees. Just like us, insects need sleep. And, like us, they have an internal sense of time – more commonly known as a body clock – which helps them synchronise their activity and sleep patterns with the rest of the world. Your body clock might allow you to wake up just a few minutes before your alarm goes off. For insects, it ensures they’re able to forage in the day when flowers are open and sleep at night when it’s usually too dark to fly.</p>
<p>Using lab-based colonies of buff-tailed bumblebees, the <a href="https://www.bumblebeeconservation.org/white-tailed-bumblebees/buff-tailed-bumblebee/">most common British bumblebee species</a>, we showed that a neonicotinoid pesticide called imidacloprid turns night into day for bees. Foraging bumblebees were fed concentrations of imidacloprid that were similar to what they might encounter in the wild (around ten parts per billion). After exposure, the dosed bees were more likely to try to forage at nighttime and sleep in the daytime, and they were more sluggish overall, going on far fewer foraging trips than normal.</p>
<p>At the same time as we were experimenting on bumblebees, we were also studying the response of fruit flies to neonicotinoids. Scientists often use fruit flies as a model to help understand other animals, as we have a deep understanding of their genes and the ability to edit them. In our study, we labelled the brain cells which set the pace of the fruit fly body clock with fluorescent dye, to see if the pesticides could be directly affecting them. </p>
<figure class="align-center ">
<img alt="A fruit fly on a piece of food." src="https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/379972/original/file-20210121-15-1xfl9dj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Fruit flies are useful for studying how chemicals affect the brain.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/fruit-fly-drosophilidae-682007272">Ant Cooper/Shutterstock</a></span>
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<p>In a normal fly, these cells collect information from the eyes and other light-sensing organs. The cells then change shape between daytime and nighttime and release signals to other parts of the body to ensure that sleep and other activities happen at the right time of day. But neonicotinoids appeared to interfere with both of these processes, freezing the body clock cells in daytime mode. Given how similar these cells are between fruit flies and bees, this process may be behind the effects on sleep and foraging that we saw in bumblebees.</p>
<h2>The environmental impact</h2>
<p>If bees can’t synchronise their foraging with the dawn, when nectar and pollen are most abundant, this will limit the amount of food they can gather, stunting the colony’s ability to grow and produce more bees. </p>
<p>The body clock is also an important part of communication in bees. Honeybees have a <a href="https://theconversation.com/follow-the-bees-dance-to-find-landscapes-green-hotspots-27004">dance language</a> which lets them tell each other where the best flowers are. They use the position of the sun in the sky as a tool for navigation, which means that honeybees need to be able to keep track of the time of day within the darkness of the hive. If their body clock is disrupted, it could affect their ability to communicate vital information to each other and reduce their ability to forage and pollinate.</p>
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Read more:
<a href="https://theconversation.com/we-discovered-more-about-the-honeybee-wake-up-call-and-it-could-help-save-them-105751">We discovered more about the honeybee 'wake-up call' — and it could help save them</a>
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<p>The changes to sleep that we saw in the buff-tailed bumblebees are also worrying. Sleep during the night helps <a href="https://jeb.biologists.org/content/215/22/3981">bees form memories</a>, and so if neonicotinoids are disrupting their sleep, it could cause problems with remembering important information, such as the route back to the hive. The correct timing of sleep is also really important for childcare in the colony. When bumblebees are looking after their young, they have to tend to them and feed them round the clock, taking little naps between feeds. If neonicotinoids change their sleep patterns in a way that they can’t control, adult bumblebees may struggle to properly care for the next generation. All of these effects could potentially prevent colonies from growing and reproducing properly, threatening their long-term survival.</p>
<p>Bumblebees, like honeybees and other bees, are important pollinators for <a href="https://repository.rothamsted.ac.uk/item/8704y/the-dependence-of-crop-production-within-the-european-union-on-pollination-by-honey-be">84% of crops</a> and <a href="https://www.cbd.int/agro/peer_review_pollinators.pdf">80% of wild flowering plants</a> in Europe. Neonicotinoids pose a real threat to not only the health of these pollinating insects, but the agriculture and ecosystems they support. As a scientist who studies the effects of these chemicals, I hope that the “emergency use” that was recently granted by the UK government isn’t a sign of worse things to come.</p><img src="https://counter.theconversation.com/content/153673/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Kiah Tasman receives funding from BBSRC. </span></em></p>Chemicals banned in the EU were recently granted an exemption for limited use in the UK.Kiah Tasman, Teaching Associate in Physiology, Pharmacology and Neuroscience, University of BristolLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1369522020-04-30T19:48:18Z2020-04-30T19:48:18ZKnow your target: Fundamental science will lead us to coronavirus vaccines<figure><img src="https://images.theconversation.com/files/330537/original/file-20200426-163083-1jdlwlp.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C4089%2C3513&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Colourized scanning electron micrograph of a cell heavily infected with SARS-CoV-2 virus particles.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/niaid/49727967917/">(The National Institute of Allergy and Infectious Diseases/Flickr)</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>The current pandemic, and maybe even more importantly the next one, will be beaten in the laboratory by strong fundamental science that informs smart medical responses and public policy.</p>
<p>Globally, the research community is galvanized to fight this virus: researchers are developing ways to <a href="https://ipac-canada.org/reprocessing-of-ppe.php">reuse personal protective equipment</a>, <a href="https://www.canada.ca/en/health-canada/services/drugs-health-products/covid19-clinical-trials/list-authorized-trials.html">devising better treatments for people who have been infected</a>, <a href="https://theconversation.com/what-scientists-are-doing-to-develop-a-vaccine-for-the-new-coronavirus-131255">creating vaccines</a> and <a href="https://www.niaid.nih.gov/news-events/nih-clinical-trial-remdesivir-treat-covid-19-begins">trying to understand what makes this virus so deadly</a>. </p>
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Read more:
<a href="https://theconversation.com/what-the-coronavirus-does-to-your-body-that-makes-it-so-deadly-133856">What the coronavirus does to your body that makes it so deadly</a>
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<p>One of the major issues in fighting the COVID-19 pandemic is that we simply don’t understand why SARS-CoV-2 — the coronavirus that causes the disease — is so dangerous. We do know that its deadly nature is a function of small genetic changes, called mutations, which distinguish it from other viruses. But which mutations? </p>
<p>SARS-CoV-2 is a <a href="https://doi.org/10.1016/j.jmb.2020.04.009">close relative of SARS-CoV</a>, the virus that caused the 2003 SARS outbreak, but even between these closely related viruses there are around 6,000 genetic differences (a staggering 20 per cent of the genome). Between these two SARS viruses and other, far less deadly coronaviruses there are even more mutations.</p>
<h2>Deadly variations</h2>
<p>Which of these changes, or combination of these changes, makes SARS-CoV-2 so deadly? This virus has <a href="https://doi.org/10.1016/j.chom.2020.02.001">14 genes in its genome, coding for 27 proteins</a>. Proteins are chains of amino acids and those 6,000 genetic differences result in 380 amino acid changes. It’s the changes in amino acids, and what those changes do to protein function, that give each virus its unique character.</p>
<p>SARS-CoV-2 is, like other coronaviruses, a sphere with spikes radiating out of it. In electron microscope images, these spikes form a crown — the corona that gives these viruses their name. In infection, the spikes attach to human cells and control the virus genes entering the cells. Different coronavirus spikes bind to different receptors on the cell surface. SARS-CoV-2 and SARS-CoV, for example, <a href="https://doi.org/10.1038/s41586-020-2180-5">bind to different receptors than the MERS virus</a>, resulting in different pathologies.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/330536/original/file-20200426-163088-4ixj9z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
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<span class="caption">Transmission electron micrograph of SARS-CoV-2 virus particles, with the corona visible.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/niaid/49645120251/">(National Institute of Allergy and Infectious Diseases/Flickr)</a></span>
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<p>Every virus has its own form of these spikes, and this large amount of variation in these spikes is a challenge to, and possible solution for, creating a SARS-CoV-2 vaccine. Vaccines work by training your immune system to recognize an antigen, <a href="https://www.cdc.gov/vaccines/hcp/conversations/downloads/vacsafe-understand-color-office.pdf">a specific aspect of an invader</a>. </p>
<p>A challenge for creating a SARS-CoV-2 vaccine, or any vaccine, is that because virus surfaces vary so much, antigens change and a vaccine for one virus doesn’t recognize another. But, if we can identify something that we know is on the surface of a virus, we can possibly create a vaccine to that antigen. With SARS-CoV-2, its unique spike is just such a possible candidate and <a href="http://doi.org/10.1126/science.abb2507">work characterizing the spike is underway</a>.</p>
<h2>Spiky science</h2>
<p>Why do different spikes have different biology? The spikes are proteins, and the differences in spike binding and shape are a function of amino acid changes, but we don’t know which ones. In part, our lack of understanding reflects our ignorance of how amino acid changes affect protein shape and function. This is where fundamental science comes in.</p>
<p>My research group studies how amino acid substitutions change protein function and biology: the exact thing we do not understand about the variation in SARS-CoV-2. We study a protein called malic enzyme which converts the chemical compound malate to pyruvate in essentially all living organisms, including <em>Drosophila melanogaster</em>, the fruit fly we work with. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=612&fit=crop&dpr=1 600w, https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=612&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=612&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=769&fit=crop&dpr=1 754w, https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=769&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/331506/original/file-20200429-51495-19r2k6u.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=769&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Drosophila melanogaster seen under a microscope at the Merritt Lab.</span>
<span class="attribution"><span class="source">(Michelle Eng)</span>, <span class="license">Author provided</span></span>
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</figure>
<p>Like every protein, <em>Drosophila</em> malic enzyme is a string of amino acids folded into a three-dimensional form. You can picture this as a ball of rubber bands — if the rubber bands were all one long string, and the ball wasn’t necessarily round. This not-round aspect is important; the shape that a protein takes depends on the amino acids in that chain. </p>
<p>A protein’s shape is determined by how its sequence of amino acids packs. Change an amino acid and you change that shape and shape determines how proteins work. This hierarchy — amino acids determine shape, shape determines function — holds whether we are looking at a metabolic enzyme or a viral spike protein. </p>
<p><em>Drosophila</em> malic enzyme is made up of almost 600 amino acids, but across the entire species, <a href="https://doi.org/10.1007/s10528-012-9523-3">only two of these ever differ</a>. At the first site, the two amino acids that we find, alanine or glycine, are fairly similar to each other, but substituting between the two actually <a href="https://doi.org/10.1007/s10528-019-09932-2">changes the enzyme’s activity by almost 30 per cent</a>, which is a big deal in biology. A closer look at this site may explain the difference in activity. </p>
<p>It is at the edge of the active site of the protein, the pocket in which the enzyme breaks down malate, and part of a helix, a twirl of amino acids forming a spiral staircase-like structure. Alanines form spirals but glycines do not. That 30 per cent difference in activity seems to result from a slightly shorter or longer spiral, a small difference leading to a subtle change in shape but very different biochemistry. </p>
<p>The second site tells a different story. At this site, the two amino acids, leucine or methionine, are also fairly similar to each other, but again we see a difference in biochemistry, <a href="https://doi.org/10.1007/s10528-019-09932-2">here about a 40 per cent difference in the strength with which the enzyme binds to malate</a>. The second site isn’t particularly near to any known structure, but is in a region of the protein in which the amino acids lie down in a sheet, interacting to form a pleated surface similar to a pleated skirt. The subtle difference between leucine and methionine likely changes the shape of this sheet, resulting in the difference in binding biochemistry.</p>
<p>Understanding both of these small differences helps us understand how amino acid variation leads to changes in protein function and gets us closer to predicting how other changes in other proteins, like a viral spike, alter their function.</p>
<h2>Foundational understanding</h2>
<p>Fundamental science is the basis of much of the work to <a href="https://www.nytimes.com/2020/04/08/health/coronavirus-vaccines.html">develop a SARS-CoV-2 vaccine</a>. Research from labs around the globe is getting us closer to beating the next pandemic. Our fly work is a small part of this process. As we get better and better at understanding protein variation, for example, we get better at designing new vaccines and possibly predicting which viruses have the potential to be deadly.</p>
<p>The COVID-19 pandemic is very unlikely to be the only such crisis we face. There are potentially <a href="http://doi.org/10.1126/science.aap7463">millions of viruses that could pose threats to humans</a>, not to mention other non-viral pathogens. Success in fighting these threats depends on strong science and strong funding for fundamental research into <a href="https://www.nytimes.com/2020/04/21/magazine/pandemic-vaccine.html">traditional and novel ways to fight infectious disease</a>.</p><img src="https://counter.theconversation.com/content/136952/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Thomas Merritt receives funding through a Discovery Grant from the Canadian Natural Sciences and Engineering Research Council. </span></em></p>Fundamental research has informed what we know about coronaviruses up until the pandemic. With possible future outbreaks, continuing and developing this type of work is crucial.Thomas Merritt, Professor, Chemistry and Biochemistry, Laurentian UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1013962018-09-03T14:01:53Z2018-09-03T14:01:53ZPutting Nigerian neuroscience research under the microscope<figure><img src="https://images.theconversation.com/files/232280/original/file-20180816-2903-8ihfer.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">Yurchanka Siarhei/Shutterstock</span></span></figcaption></figure><p>Researchers are working hard to unravel the complex mysteries of the human brain and nervous system, as well as to find treatment for often incurable brain diseases. These neuroscientists are <a href="https://www.cell.com/neuron/abstract/S0896-6273(16)30800-5">mostly based</a> in Europe, the US, Japan and China. So most of our understanding of the brain comes from the global North, with only minor contributions from places like Africa.</p>
<p>That’s not to say neuroscience isn’t being researched across the continent. But there are huge barriers to innovation and productivity. </p>
<p>Most universities <a href="https://www.weforum.org/agenda/2017/06/africa-s-scientists-are-not-absent-they-just-need-the-right-kind-of-investment-b93066ad-8320-4f69-be60-e58da659d59b/">do not have equipment</a> for scientific research. And where research is happening, it’s often being carried out using <a href="https://www.theatlantic.com/international/archive/2013/09/the-inadequacy-of-donating-medical-devices-to-africa/279855/">outdated equipment</a>. The <a href="http://www.engineeringnews.co.za/article/lack-of-reliable-power-supply-hinders-africas-growth-trade-commission-2017-03-17">lack of reliable power</a> across large stretches of the continent is another issue. This makes it difficult to acquire, use or store common materials used in biomedical research such as antibodies and tissue samples.</p>
<p>For neuroscience, a number of local and international programmes are trying to address these shortcomings. For example the <a href="http://ibro.org/">International Brain Research Organisation</a> and the <a href="https://www.neurochemistry.org/">International Society for Neurochemistry</a> have invested in the training of many scientists across Africa. Not for profit bodies like <a href="http://www.trendinafrica.org">Teaching and Research in Natural Sciences for Development in Africa</a> and <a href="https://seedinglabs.org">Seeding Labs</a> have helped in setting up laboratories in some African countries. Such efforts have helped to boost the neuroscience skills of scientists in many African countries. </p>
<p>But this hasn’t yet levelled the difference in scientific output between researchers in Africa and those in the “global North”. Perhaps bridging this gap and identify methods that could boost the continent’s neuroscience capacity, requires more knowledge about scientists’ challenges and strengths in different countries.</p>
<p>With this in mind, my colleagues and I set out to examine the state of Nigerian neuroscience. By <a href="https://osf.io/preprints/africarxiv/ahv2t/">analysing</a> more than 1,200 neuroscience extracted publications from PubMed, a free full-text archive of biomedical and life sciences journal literature, we found that Nigerian neuroscience research has its own strengths and shortcomings. </p>
<p>Only a few laboratories use modern methods. The research models used are expensive and don’t necessarily reveal a great deal, and there’s a disconnect between research findings and eventual patient care. However, Nigeria has many young, passionate neuroscientists. This means that the coming years could be exciting for neuroscience in Nigeria – if proper investments are made.</p>
<p>There’s never been an in-depth investigation of this nature. Our work can guide scientists and policy makers in making the right decisions for Nigeria’s neuroscience landscape.</p>
<h2>Shortcomings and challenges</h2>
<p>Nigeria is Africa’s <a href="https://www.worldatlas.com/articles/the-10-most-populated-countries-in-africa.html">most populous</a> nation. It’s also a hot spot for neuroscience research, <a href="https://www.sciencedirect.com/science/article/pii/S2405650215000155">third only to South Africa and Egypt</a>.</p>
<p>Some of our findings included:</p>
<ul>
<li>Nigerian researchers tend not to use affordable and powerful models for their research. For instance, many of the studies we examined were conducted using rats and mice. This makes sense, at face value: these rodent species are commonly used because of their similar genetic make up to humans.<br></li>
</ul>
<p>But it costs money to manage rodents. And, to answer research questions relevant to human diseases, these rodents need to be genetically modified to have or mimic these diseases, which makes them even more expensive. The models used in Nigerian neuroscience are not genetically modified. </p>
<ul>
<li>Only 8% of studies used many key “advanced” methods that are readily available to researchers outside Africa, such as real-time polymerase chain reaction, fluorescence or electron microscopy among others. </li>
</ul>
<p>To put this in perspective, more than half of the Nobel Prizes won in Physiology or Medicine in the past two decades employed genetically amenable models and advanced research techniques. This emphasises the importance of using advanced tools and suitable models for big discoveries. </p>
<ul>
<li>Nigerian neuroscience is also guilty of under exploiting its strengths. In Africa, medicinal plants have been used <a href="https://www.hindawi.com/journals/ecam/2013/617459/">for centuries</a> to treat disease. Nigeria, with its rich medicinal plant resources, could become a leader in the field of drug discovery.</li>
</ul>
<p>41% of all Nigerian basic neuroscience publications examined in our study set out to establish the utility of medicinal plants for future medical application. </p>
<p>It would be expected that some of these medicinal plants would be tested through clinical research. However, we found no clinical studies that used the results from the basic research or reported the benefits or toxicity from the wide use of these plants among people. This disconnect between basic and clinical research may have many consequences, such as reducing homegrown health-driven innovation.</p>
<ul>
<li>More broadly, infrastructure and training need to be properly funded.</li>
</ul>
<p>There are a few things that can be done to address these issues and better support Nigerian neuroscience. </p>
<h2>Potential solutions</h2>
<p>For starters, it’s important for Nigerian neuroscience researchers to realise there are many genetically amenable models available for their work. These models, among them fruit flies, Zebra fish and the roundworm species C. elegans, are far cheaper than rats and mice.</p>
<p>Money must be invested to equip Nigerian laboratories with modern research tools to make them globally competitive.</p>
<p>More time and money must be invested in introducing Nigerian scientists to advanced research methods. This would greatly enhance the quality of work produced in the country and drive scientific innovation in biomedical research coming from Africa. </p>
<p>Research programmes, grants and rewards need to be put in place to encourage collaboration between basic and clinical scientists. This will help to enhance the relevance of research to patient care and allow for basic research to be properly tested in a clinical setting.</p>
<p>We also hope our findings will encourage more Nigerian scientists and scientific societies to get involved in science advocacy. They need to sell what they’re doing to the public and policymakers, and explain why it should be funded.</p>
<p>In the coming months, we’ll be putting together similar research about other African countries to create a fuller picture. From there, we hope to identify targeted solutions to the challenges facing scientists in different parts of the continent.</p><img src="https://counter.theconversation.com/content/101396/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Mahmoud Bukar Maina PhD FRSA receives funding from The Physiological Society, The Biochemical Society, British Pharmacological Society and University of Sussex for his public engagement work in Africa. However they are not involved, and neither was the work that led to this article funded. He is affiliated with TReND in Africa (<a href="http://www.TReNDinAfrica.org">www.TReNDinAfrica.org</a>) and Science Communication Hub Nigeria (<a href="http://www.scicomnigeria.org">www.scicomnigeria.org</a>)</span></em></p>With the right investment, the next few years could be extremely exciting for Nigerian neuroscience.Mahmoud Bukar Maina FRSA, Research Fellow, University of SussexLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/991592018-07-02T15:47:46Z2018-07-02T15:47:46ZHow adapting to different climates has helped a pest spread across the globe<figure><img src="https://images.theconversation.com/files/225497/original/file-20180629-117430-yf96qh.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The Mediterranean fruit fly, Ceratitis capitata.</span> <span class="attribution"><span class="source">Andre Coetzer</span></span></figcaption></figure><p>If you have ever bitten into a fruit and been disgusted to find it wriggling with cream-coloured maggots, you have already met at least one member of the fruit fly family. </p>
<p>True fruit flies belong to the fly family <a href="https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/tephritidae">Tephritidae</a>, and are quite different from the small <em>Drosophila</em> or “vinegar flies” that hover around and drown in your glass of wine. Unlike <em>Drosophila</em>, which lay their eggs in decaying organic matter such as fruit in a bowl in your kitchen, true fruit flies lay their eggs in ripening fruit that’s developing on the tree. </p>
<p>Once the larvae hatch, they feed on the fruit they were laid in. The damage caused by this larval feeding means that true fruit flies are trouble for fruit growers. Farmers often turn to costly control tactics to try and prevent infestation by true fruit fly larvae, reducing their profits. And fruit infested with true fruit fly larvae can’t be exported. This pest costs fruit farmers and governments <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0111582">well over US$1 billion each year</a>. </p>
<p>The Mediterranean fruit fly, <em>Ceratitis capitata</em>, is among the most destructive true fruit flies in the world. It is <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/ddi.12333">native to Africa</a> but is now found in countries around the Mediterranean Basin and Middle East, South and Central America, and parts of Australia and the US. What’s remarkable about this almost global distribution is the wide range of climates that the Mediterranean fruit fly has been able to colonise and thrive in. </p>
<p>My colleagues and I set out <a href="https://www.nature.com/articles/s41598-018-28259-3#article-info">to study</a> how this little pest has managed to spread over such wide-ranging environments. We found that the Mediterranean fruit fly is highly adaptable to different environments and can survive extremes in temperature, and water and food availability.</p>
<h2>Environmental stress tests</h2>
<p>All insects are ectotherms. This means that their body temperature and all life processes – movement, digestion, growth, development and reproduction – are determined by the temperature around them. Water and food availability are also important for survival and growth. </p>
<p>We measured the ability of Mediterranean fruit flies from different climates across South and East Africa to survive high and low temperatures, as well as a lack of water or food. We collected infested fruit from eight sites in South Africa and Kenya, then held the developing larvae and pupae under common environmental conditions in the laboratory. The adult flies were then used in experiments.</p>
<p>First we transferred flies from each site to different temperatures. This is because prior exposure of the Mediterranean fruit fly (as well as other insects) to a warmer or cooler temperature <a href="https://www.sciencedirect.com/science/article/pii/S0306456511001136">improves their survival</a> when it comes to tolerating extreme temperatures.</p>
<p>We also wanted to know whether closely related populations responded to environmental stress more similarly than populations that were more distantly related. We built a <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/phylogenetic-trees">phylogenetic tree</a> based on the genetic fingerprint of each population. Then we compared populations taking into account how closely they were related and the climate they were sampled from.</p>
<p><a href="https://www.nature.com/articles/s41598-018-28259-3">Our results</a>, recently published in the open access journal <em>Scientific Reports</em>, showed that the Mediterranean fruit fly is highly adaptable. </p>
<p>The eight populations we sampled showed different patterns in their ability to survive high and low temperatures, and lack of water or food. The results lead us to believe that each population adapts differently to its local environment. </p>
<p>In addition, all populations exhibited some flexibility in their environmental tolerance as a result of the temperatures they had experienced before testing. If flies had experienced cooler temperatures before testing, their tolerance of cold temperatures was improved but they were less able to withstand high temperatures. Prior experience of warmer temperatures led to improved tolerance of high temperatures and reduced tolerance of cold temperatures.</p>
<h2>An adaptable pest</h2>
<p>Our research suggests that the Mediterranean fruit fly has been able to leave its native Africa and become a globally invasive fruit production pest
because of its ability to adapt rapidly to new environments. </p>
<p>Its ability to evolve rapidly to different environmental conditions also suggests that the Mediterranean fruit fly will be well suited to cope with climate change.</p>
<p>Short of using pesticides, which are expensive, there are other steps farmers can take to limit the numbers and spread of the Mediterranean fruit fly. Harvested fruit should be inspected and sorted to prevent infested fruit from reaching markets. Temperature or radiation treatments can also be applied to kill larvae in the fruit.</p>
<p>For countries not currently affected by the Mediterranean fruit fly, it is vital to prevent its entry and establishment by enforcing stringent quarantine regulations.</p>
<p>In both cases, government agencies and grower collectives need to provide support required to limit the economic damage caused by this adaptable pest.</p><img src="https://counter.theconversation.com/content/99159/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Christopher Weldon receives funding from the South African National Research Foundation and Citrus Research International. He is affiliated with and is the current elected President of the Entomological Society of Southern Africa. </span></em></p>The Mediterranean fruit fly can evolve rapidly to different environmental conditions, this suggests it will be well suited to cope with climate change.Christopher Weldon, Senior Lecturer in Entomology, University of PretoriaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/963222018-05-23T22:53:45Z2018-05-23T22:53:45ZDavid Suzuki backlash ignores his prize-worthy science<figure><img src="https://images.theconversation.com/files/220200/original/file-20180523-51135-u2jqpl.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">David Suzuki is an environmental activist, broadcaster and globally recognized geneticist.</span> <span class="attribution"><a class="source" href="https://davidsuzuki.org">David Suzuki Foundation</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>When the University of Alberta announced it would award David Suzuki an honorary doctor of science degree at its spring convocation, <a href="https://www.thestar.com/edmonton/2018/04/23/law-firm-pulls-donation-from-university-of-alberta-as-suzuki-backlash-continues.html">there was (and continues to be) a vocal backlash</a>. </p>
<p>Critics argue his stance against Alberta’s oil sands make him an unsuitable recipient. Although <a href="https://www.ualberta.ca/why-ualberta/administration/chancellor-and-senate/honorary-degrees/current-honorary-degree-recipients">Suzuki is receiving the honour because of his efforts to boost science literacy and environmental awareness</a>, it’s important to remember that before he became a broadcaster and an activist, he was a globally recognized scientist.</p>
<p>Born in Vancouver in 1936, David Suzuki and his family (all Canadian-born citizens) were subjected to the unethical Japanese internment during the Second World War. The Canadian government sold the family’s dry cleaning business, <a href="http://learning.royalbcmuseum.bc.ca/entries/david-suzuki-talks-about-his-familys-internment-in-wwii/">interned them and sent Suzuki’s father to a labour camp</a>.</p>
<p>Despite these setbacks, Suzuki embarked on a career in science with his first professorial appointment in the genetics department at the University of Alberta in 1962.</p>
<p>Today, as a dedicated scientist and communicator of science, Suzuki frequently presents the <a href="https://davidsuzuki.org/story/cant-close-eyes-climate-change/">scientific case for climate change and the effect of fossil fuels</a> to the public. No other scientist in Canada has been <a href="http://www.cbc.ca/radio/thecurrent/the-current-for-april-26-2018-1.4636157/david-suzuki-should-not-be-celebrated-in-alberta-says-former-dragons-den-star-1.4636160">pilloried so strongly for simply presenting the data</a>.</p>
<h2>A Nobel nod</h2>
<p>While many may think of Suzuki as an activist or a <a href="http://www.cbc.ca/natureofthings/">television presenter</a>, he also holds a legacy in genetics research that contributes to the foundation of knowledge and advances in the life sciences.</p>
<p>Jeffrey Hall, professor emeritus of biology at Brandeis University in Waltham, Mass., was part of a trio of scientists <a href="https://www.nobelprize.org/nobel_prizes/medicine/laureates/2017/hall-facts.html">awarded the Nobel Prize in Physiology or Medicine in 2017</a> for their work on discovering the molecular mechanism behind circadian rhythms, the body’s internal clock. </p>
<p><a href="https://www.cell.com/fulltext/S0960-9822(07)02369-X">In an interview prior to this recognition</a>, Hall was asked: “Do you have any other ‘heroes,’ as it were, among researchers in your field?” Hall identified Suzuki as one: “The genetic world reacted to Suzuki’s approach and accomplishments as if they were genuinely sensational.” </p>
<p>So what was this breakthrough made decades ago by Suzuki at the front lines of genetics research? </p>
<p>As a professor at the University of British Columbia, Suzuki wanted to understand how muscle worked and tried to uncover genes that would cause paralysis. He reasoned that such genes would be in common to all life forms with muscle. He selected the common fruit fly, <em>Drosophila melanogaster</em>, for his experiments.</p>
<p>This was genius! </p>
<h2>Suzuki’s discovery</h2>
<p>It’s worth highlighting the beauty of Suzuki’s strategy because this legacy and approach has stood the test of time. </p>
<p>Until that time, research on fruit flies was considered esoteric and narrow. In Hall’s view, Suzuki’s “work was crucial to the resurrection of <em>Drosophila</em> from the ash heap of biological research.” </p>
<p>Suzuki’s experimental design was elegant and conclusive. He simply fed fruit flies a chemical known to cause random mutations. </p>
<p>In 1967, Suzuki was the first to use temperature to screen for genetic mutations in fruit flies. These temperature-sensitive mutants behaved normally when the flies were kept near room temperature (22°C). The effects of the mutation were only observed at a higher temperature (29°C), <a href="http://science.sciencemag.org/content/170/3959/695.long">he later wrote in <em>Science</em></a> magazine.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/220017/original/file-20180522-51121-1o3tfwo.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">The fruit fly Drosophila melanogaster is a model organism used to understand the biology of other organisms, including humans.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/drosophila-melanogaster-fruit-fly-extreme-close-322358456?src=tYx4Fzi1Y4PKJK12lsjXXA-1-7">(Shutterstock)</a></span>
</figcaption>
</figure>
<p>At the high temperature, some of the flies became paralyzed and fell to the bottom of their container, while unaffected ones simply flew. When he changed the temperature to 22°C, a small number of the paralyzed fruit flies at the bottom of the container regained the ability to fly. </p>
<p>The flies’ recovery after the temperature change meant they harboured a mutation in a single gene. Suzuki named the gene “shibire,” the Japanese word for “paralyzed.”</p>
<h2>A dynamic outcome</h2>
<p>Other scientists determined the shibire gene codes for <a href="https://www.sciencedirect.com/science/article/pii/095943889580059X?via%3Dihub">a protein named dynamin that controls small structures found at the junction between nerve and muscle</a> that house the chemicals necessary for muscle contraction. A mutation in shibire prevents muscle contraction and results in paralysis. In humans, such mutations are linked to <a href="https://www.nature.com/articles/ng0305-215">neurodegenerative diseases</a>, including Charcot-Marie-Tooth disease. </p>
<p>Today, about 5,000 scientific publications on dynamin reveal a function common to all life forms with nuclei in their cells — that is all animals, plants, yeast, flies, etc. </p>
<p>Suzuki went on to show several examples of mutations in single genes. The second gene Suzuki discovered was named “stoned,” since the flies had unco-ordinated wing and leg movement. Today, we understand that <a href="http://www.jneurosci.org/content/19/14/5847.long">this gene encodes for a protein that also affects the same fundamental machinery as dynamin</a>.</p>
<p>It was not long before the international community of discovery researchers followed Suzuki’s lead. He had correctly predicted that studying genetic mutations in fruit flies could help scientists identify genes involved in the development of human disease and other phenomena. </p>
<p>History will judge the outcome of Suzuki’s attempt to use observation and reason to <a href="https://www.folio.ca/commentary--energy-industry-must-not-be-allowed-to-bully-universities">“advance scientific literacy, appreciation of nature and knowledge of the ecological crises threatening life on the planet.”</a> </p>
<p>But it remains that Suzuki may be considered Canada’s pioneer in fundamental genetics research.</p>
<p><em>John Bergeron gratefully acknowledges Kathleen Dickson as co-author.</em></p><img src="https://counter.theconversation.com/content/96322/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>John Bergeron does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>David Suzuki may be best known as an environmental activist and the face of CBC’s ‘The Nature of Things,’ but he’s also a globally recognized scientist.John Bergeron, Emeritus Robert Reford Professor and Professor of Medicine at McGill, McGill UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/933262018-03-16T14:51:52Z2018-03-16T14:51:52ZHave we got the causes of type 2 diabetes wrong?<figure><img src="https://images.theconversation.com/files/210607/original/file-20180315-104699-705w3i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/555870082?src=BxuSbkmpKaXwsVHIiSpraQ-1-2&size=medium_jpg">Montri Thipsorn/Shutterstock.com</a></span></figcaption></figure><p>The proportion of adults with diabetes around the world has risen from 4.7% in 1980 to more than <a href="http://www.who.int/mediacentre/factsheets/fs312/en/">8.5% today</a>. More than 422m people now suffer from diabetes – so there is an urgent need to better understand the disease and develop new treatments. However, new research from Heidelberg University in Germany suggests that we may have got the causes of type 2 diabetes wrong. But have we? And if so, how might it affect treatment? </p>
<p>People with diabetes need to carefully monitor their blood-sugar levels. This is important, as it helps to reduce the risk of developing complications, such as heart disease and blindness. But even with good control of blood-sugar levels, people with diabetes often go on to develop further complications, including nerve damage and kidney damage. This suggests that effective treatment of diabetes requires more than simply good control of blood-sugar levels.</p>
<p>Type 2 diabetes – often associated with obesity – happens when the pancreas doesn’t release enough of the hormone, insulin, or the body’s cells don’t react to insulin. (Insulin helps the body use glucose for immediate energy needs or store it for future energy needs.) This means that sugar (glucose) stays in the blood and isn’t used as fuel for energy. The cause of these defects remains controversial.</p>
<p>The latest research, published in <a href="http://www.cell.com/cell-metabolism/fulltext/S1550-4131(18)30114-1">Cell Metabolism</a>, suggests that a molecule called methylglyoxal (MG) may cause many of the defects associated with type 2 diabetes. But what does it do?</p>
<p>MG is a reactive metabolite (a byproduct of cells) that leads to the formation of other powerful molecules that are readily able to modify protein, fats and DNA in cells. This typically prevents those molecules from working – and this can then result in cells no longer functioning properly. These events are known to lead to the development of diseases such as <a href="https://www.nhs.uk/conditions/atherosclerosis/">atherosclerosis</a>, which can trigger strokes and heart attacks.</p>
<p>MG is formed as a result of metabolic pathways – a linked series of chemical reactions occurring in a cell – that are overactive in diabetes and obesity. So it was previously thought that MG production was the result of obesity and diabetes. However, this new research suggests that MG might also contribute to the development of these conditions. </p>
<p>Using genetic engineering, the researchers turned off the enzyme that breaks down MG in flies. MG then accumulated in their bodies and the flies developed insulin resistance. Later they became obese and as time went on their glucose levels subsequently also became disrupted. </p>
<p>These new findings might help explain why, even with good control of blood-sugar levels, diabetic complications still develop. There are important implications from this work, as this suggests that it might be possible to slow down – or even prevent – diabetes complications from developing through a combination of good glucose control along with MG reduction. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=475&fit=crop&dpr=1 600w, https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=475&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=475&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=597&fit=crop&dpr=1 754w, https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=597&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/210605/original/file-20180315-104650-9pey9e.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=597&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">An obese fruit fly from the experiment. Its body fat glowing with green fluorescence.</span>
<span class="attribution"><span class="source">Aurelio Teleman</span></span>
</figcaption>
</figure>
<h2>What does it mean for diabetes treatment?</h2>
<p>While diabetes treatments are often effective at bringing blood-sugar levels down, over time their effectiveness usually decreases. As such there is an urgent need to develop new drugs that work to control diabetes and its complications in different ways.</p>
<p>Most current strategies aim to stop the development of type 2 diabetes by targeting cells and tissues linked to insulin secretion from the pancreas, glucose uptake into cells, or by preventing glucose release from stores in the liver. Together these strategies can help control blood-sugar levels.</p>
<p>The new research, however, suggests that in addition to controlling blood-sugar levels we should also consider additional treatments that work by preventing reactive metabolites, such as MG, from forming. But what would be the best way to achieve this?</p>
<p>Reactive metabolites can lead to extensive damage within cells. There is good news, though, in that there are molecules that can effectively stop these products from forming. </p>
<p>Antioxidants, such as vitamin C and vitamin E, have previously been suggested as possible diabetes treatments. However, studies using this approach have had mixed results. One possible explanation for this is that there are multiple reactive metabolites, not all of which are sensitive to antioxidants.</p>
<p>A new champion may now have emerged, though, in the form of the naturally occurring nutritional supplement called carnosine. This is a molecule that was <a href="https://www.nature.com/articles/s41598-017-13649-w">recently shown</a> to prevent formation of numerous reactive metabolites that are formed from glucose and fatty acids.</p>
<p>Clinical trials are ongoing, but <a href="http://onlinelibrary.wiley.com/doi/10.1002/oby.21434/abstract">initial findings are promising</a>. They <a href="https://www.sciencedirect.com/science/article/pii/S0271531717303652?via%3Dihub">suggest that</a> <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0138646">carnosine is able to reduce blood-sugar levels</a>, as well as <a href="https://www.nature.com/articles/srep44492">prevent</a> <a href="https://link.springer.com/article/10.1007%2Fs00125-014-3467-6">multiple complications</a> that are <a href="https://www.tandfonline.com/doi/abs/10.1185/03007995.2015.1037731?journalCode=icmo20">associated with diabetes</a>. Even better, as this is classified as a dietary supplement rather than a drug, no prescription is needed in order to take carnosine.</p><img src="https://counter.theconversation.com/content/93326/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Mark Turner receives funding from the British Council in the form of a grant entitled "Carnosine: biological actions and therapeutic implications". </span></em></p>A new study suggests that high blood-sugar levels are an effect rather than a cause of type 2 diabetes.Mark Turner, Associate Professor, Nottingham Trent UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/850342017-10-05T12:06:47Z2017-10-05T12:06:47ZThe ancient clock that rules our lives – and determines our health<figure><img src="https://images.theconversation.com/files/188765/original/file-20171004-18533-1vz6v53.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/440570470?size=medium_jpg">Vadim Sadovski/Shutterstock</a></span></figcaption></figure><p>Our lives are ruled by time; we use time to tell us what to do. But the alarm clock that wakes us in the morning or the wristwatch that tells us we are late for supper are unnatural clocks. Our biology answers to a profoundly more ancient beat that probably started to tick early in the evolution of all life. </p>
<p>Embedded within the genes of us, and almost all life on earth, are the instructions for a <a href="https://global.oup.com/ukhe/product/circadian-rhythms-a-very-short-introduction-9780198717683?cc=gb&lang=en&">biological clock</a> that marks the passage of around 24 hours. Biological clocks or “circadian clocks” help time our sleep patterns, alertness, mood, physical strength, blood pressure and much more. </p>
<p>Under normal conditions, we experience a 24-hour pattern of light and dark, and our circadian clock uses this signal to align biological time to the day and night. The clock is then used to anticipate the differing demands of the 24-hour day and fine-tune physiology and behaviour in advance of the changing conditions. Body temperature drops, blood pressure decreases, cognitive performance drops and tiredness increases in anticipation of going to bed. While before dawn, metabolism is geared-up in anticipation of increased activity when we wake. </p>
<p>A circadian clock also stops everything happening at the same time, ensuring that biological processes occur in the appropriate sequence. For cells to work properly they need the right materials in the right place at the right time. </p>
<p>Thousands of genes have to be switched on and off in order and in harmony. Proteins, enzymes, fats, carbohydrates, hormones, nucleic acids and other compounds have to be absorbed, broken down, metabolised and produced in a precise time window. Energy has to be obtained and then allocated to growth, reproduction, metabolism, locomotion and cellular repair. </p>
<p>All of these processes, and many others, take energy and all have to be timed to the correct time of the day. Without a clock, our biology would be in chaos. </p>
<p>The <a href="https://www.nobelprize.org/nobel_prizes/medicine/laureates/2017/press.html?utm_source=twitter&utm_medium=social&utm_campaign=twitter_tweet">pioneering research</a> of Jeffrey Hall, Michael Rosbash and Michael Young – awarded the <a href="https://www.nobelprize.org/nobel_prizes/medicine/laureates/2017/">2017 Nobel Prize in Physiology or Medicine</a> earlier this week – provided our first clear understanding of how a biological clock ticks in any organism; in this case, a fruit fly. </p>
<h2>How the clock works</h2>
<p>At the heart of the clock is a “negative feedback loop” which consists of the following sequence of events. The clock genes produce messages that are translated into proteins. The proteins then interact to form complexes and move from the cytoplasm of the cell into the nucleus and then inhibit their own genes. These inhibitory clock protein complexes are then broken down and the clock genes are then once more free to make more messages and fresh protein – and the cycle continues day after day.</p>
<p>This negative feedback loop generates a near 24-hour rhythm of protein production and degradation that drives the internal biological day. </p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"914786230658887680"}"></div></p>
<p>Based on the findings of Hall, Rosbash and Young in the fruit fly, very similar clock genes were then discovered in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815553/">mice</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/12452483">humans</a> and many other animals. So the biological clocks that “tick” in us are broadly similar to the clocks found in insects, worms, fish and birds. </p>
<p>We now know that the morning and evening preferences of individuals who describe themselves as either “larks” or “owls” also appear to be related to <a href="http://www.cell.com/cell/fulltext/S0092-8674(17)30346-X">small changes in some of these clock genes</a> that either speed up or slow down our circadian rhythms. </p>
<h2>Do not disturb</h2>
<p>An understanding of how circadian clocks work and the central role they play in our biology has led to advances in many areas, not least an appreciation that when circadian rhythms are disrupted our overall health and well-being can be severely affected. </p>
<p>Shift workers try to sleep during the day, but sleep is usually shorter and of poorer quality than when sleep occurs at night because, although desperately tired, the circadian system is instructing the body that it should be awake. They then work during the night at a time when the circadian system has prepared the body for sleep, and alertness and performance are low. In effect, they work when they are sleepy and sleep when they are not. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/188585/original/file-20171003-31655-rfi7sa.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Working shifts has serious implications for your health.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/568203484?src=Ev4HJSl8NPatGoGgfgki-Q-1-1&size=medium_jpg">Dmitry Bunin/Shutterstock</a></span>
</figcaption>
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<p>Short-term circadian rhythm disruption can have a big negative impact on <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656292/">memory</a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656292/">problem solving</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/24639663">emotional responses</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656292/">attention</a>. And years of night-shift work has been shown to increase the risk of <a href="http://www.bmj.com/content/355/bmj.i5210.long">heart disease</a>, <a href="http://www.thedoctorwillseeyounow.com/content/autoimmune/art2361.html">infection</a>, <a href="http://www.sjweh.fi/show_abstract.php?abstract_id=3666">cancer</a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370346/">type 2 diabetes</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370346/">obesity</a>. So we ignore our circadian rhythms at our peril. </p>
<p>Circadian rhythm disruption is also a feature shared by some of the most challenging diseases of our time. Sufferers of mental illnesses such as <a href="https://www.ncbi.nlm.nih.gov/pubmed/22194182">schizophrenia</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/28902457">bipolar disorder</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/28902457">depression</a>; neurological conditions like <a href="https://www.ncbi.nlm.nih.gov/pubmed/28890168">Alzheimer’s</a>, <a href="http://www.bmj.com/content/355/bmj.i5210.long">stroke</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/25698167">multiple sclerosis</a>; developmental disorders such as <a href="https://www.ncbi.nlm.nih.gov/pubmed/28902457">autism</a>; and serious disorders of the eye (<a href="http://iovs.arvojournals.org/article.aspx?articleid=2128937">including the development of cataracts</a>) all exhibit circadian-rhythm disruption. </p>
<p>The future of circadian rhythms research is to understand how this disruption comes about, and, based on this knowledge, develop new drugs and treatments that will help us regulate internal time across the health spectrum. We truly live in exciting times.</p><img src="https://counter.theconversation.com/content/85034/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Russell Foster receives funding from BBSRC and Wellcome Trust.</span></em></p>Biological clocks set the pace for nearly all living things, and Jeffrey Hall, Michael Rosbash and Michael Young – awarded the Nobel Prize in Physiology or Medicine – helped us understand how.Russell Foster, Professor of Circadian Neuroscience, University of OxfordLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/850612017-10-03T02:29:40Z2017-10-03T02:29:40ZNobel winners identified molecular ‘cogs’ in the biological clocks that control our circadian rhythms<figure><img src="https://images.theconversation.com/files/188462/original/file-20171003-12163-1cgw877.jpg?ixlib=rb-1.1.0&rect=414%2C0%2C3835%2C2459&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">'The key fourth awardee here is ... the little fly,' Hall said.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/oregonstateuniversity/8725460037">Lynn Ketchum</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>Circadian rhythms control when we’re at our peak performance physically and mentally each day, keeping our lives ticking in time with Earth’s day/night cycle. This year’s Nobel Prize in Physiology or Medicine was <a href="https://www.nobelprize.org/nobel_prizes/medicine/laureates/2017/press.html">awarded to three American scientists</a>, Jeffrey Hall and Michael Rosbash of Brandeis University and Michael Young of Rockefeller University, for shedding light on how time is measured each day in biological systems, including our own bodies.</p>
<p>From Darwin’s finches on the Galápagos Islands to modern city dwellers, organisms adapt to their environment. Regular 24-hour cycles of day and night on Earth led to the evolution of biological clocks that reside within our cells. These clocks help us unconsciously pick the best time to rest, search for food, or anticipate danger or predation.</p>
<p>The field of modern circadian biology got its start in the 1970s, when geneticist Seymour Benzer and his student Ron Konopka undertook a revolutionary study to track down the genes that encode biological timing in fruit flies. With that gene in their sights, the labs of Hall, Rosbash and Young ushered in the molecular era of circadian biology as they untangled the molecular mechanisms of biological timekeeping.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=294&fit=crop&dpr=1 600w, https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=294&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=294&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=370&fit=crop&dpr=1 754w, https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=370&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/188468/original/file-20171003-12146-1i5swxs.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=370&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption"><em>Drosophila</em> larvae were the lab subject for the early circadian clock research.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/larvae-drosophila-flies-test-tube-nutrient-93720691">IrinaK/Shutterstock.com</a></span>
</figcaption>
</figure>
<h2>Why flies?</h2>
<p>To get started, Benzer and Konopka performed a simple experiment: tracking when the fruit fly <em>Drosophila melanogaster</em> would emerge from its pupal case. This developmental process, called eclosion, served as a powerful tool to study the complicated biological process of circadian rhythms. Because <em>Drosophila</em> pupae emerge only at a specific time of the day, Konopka could measure the timing between rounds of eclosion for different strains of flies and identify those that had a bad clock. By isolating fly strains with timing problems, they hoped to be able to zero in on the relevant genes that controlled this internal clock.</p>
<p>In the end, Konopka found three mutant strains: one that had a short, 19-hour day; one with a long, 28-hour day; and one mutant that appeared to have no clock at all. Using genetic tools, he was able to show that each of the responsible mutations lay remarkably close on the same chromosome, suggesting that they were all located within a single gene, <a href="http://www.pnas.org/content/68/9/2112.short">which Benzer and Konopka named <em>period</em></a> for its apparent control over clock timing.</p>
<p>Then the race was on, and in 1984, two teams finally identified this so-called clock gene <em>period</em> in flies: the labs of <a href="https://doi.org/10.1016/0092-8674(84)90015-1">Jeffrey Hall and Michael Rosbash</a> working in close collaboration at Brandeis, <a href="https://doi.org/10.1038/312752a0">and Michael Young’s</a> lab at Rockefeller.</p>
<p>With the gene in hand, these groups then aimed to figure out how <em>period</em> fit into a biological clock. The first clue came when Jeffrey Hall and Michael Rosbash discovered that <a href="https://doi.org/10.1016/0896-6273(88)90198-5">the protein encoded by this gene (called PER)</a> increased during the night and decreased during the day, suggesting that levels of the protein might somehow communicate time information to the rest of the cell. </p>
<h2>Biological loops and timers</h2>
<p>If you just imagine how a biological clock might best keep track of time over a day, you might jump to a mental picture of an hourglass timer. Sand gradually disappears over time; when all the sand is gone, it could signal the process to begin again. Was PER the substance that kept biological time by gradually changing throughout the day?</p>
<p>One key insight came when Hall and Rosbash reasoned that this PER protein might actually block the activity of the <em>period</em> gene, <a href="https://doi.org/10.1038/343536a0">turning itself off each day</a>. As levels of PER build up over the course of the night, less and less new PER protein would be made. Eventually the protein levels drop and the process starts over again. This is called a negative feedback loop. It’s the same type of biological balancing act that keeps everything from your blood sugar levels to your circadian rhythms in line throughout your body. </p>
<p>This kind of negative feedback system is similar to how a thermostat controls the temperature of a room. If the temperature drops below the set point, the thermostat turns on the heater. When the room gets too toasty, the thermostat turns off the furnace. Here, negative feedback – a buildup of heat – works to control the heater and maintain a constant temperature.</p>
<p>Now imagine having to repeat this process over and over each day with nearly exact timing. Biological clocks use negative feedback from clock proteins like <em>period</em> to turn themselves on and off again each 24 hours. Additional studies in the Young lab identified other key genes – dubbed <em><a href="https://doi.org/10.1126/science.8128247">Timeless</a></em> and <em><a href="https://doi.org/10.1016/S0092-8674(00)81224-6">Double-Time</a></em> – that fit into this puzzle by controlling how PER travels around the cell to turn itself off each day. </p>
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<a href="https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=565&fit=crop&dpr=1 754w, https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=565&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/188467/original/file-20171003-12115-1gmh23w.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=565&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Piece by piece, starting to understand the biological mechanisms of our living clockworks.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/wwarby/11271766325">William Warby</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<h2>Fitting the cogs together into molecular clocks</h2>
<p>Work over the last two decades has rounded out a much deeper understanding of circadian rhythms to show how most organisms have clocks based on feedback loops similar to <em>Drosophila</em>. Rosbash’s lab identified part of the PER protein <a href="https://doi.org/10.1038/364259a0">known as the PAS domains</a> that we now find in many clock proteins from fungi and plants to humans. PAS domains help clock proteins like PER <a href="https://doi.org/10.1126/science.7855598">pair up with their partners</a> to control the negative feedback loop.</p>
<p>By <a href="https://doi.org/10.1371/journal.pbio.1000094">comparing differences in the structures</a> of PER PAS domains of <em>Drosophila</em> and mice, scientists are now beginning to learn how the protein “cogs” of the molecular clock fit together to tell time. Understanding circadian rhythms at atomic resolution like this allows us to explain how newly identified mutations in PER <a href="https://doi.org/10.1073/pnas.1517549113">lead to changes in clock timing</a> and open the door to therapeutics that could harness the power of circadian rhythms to improve human health.</p>
<h2>Living with your clock and its natural rhythms</h2>
<p>We now have a much greater appreciation for the central role that circadian rhythms play in coordinating our lives with Earth’s day, controlling everything <a href="https://doi.org/10.1016/j.cub.2016.04.011">from your metabolism to the timing of sleep</a>. Young’s lab recently identified a prevalent mutation in a human clock gene, <em>cryptochrome 1</em>, that lengthens the cellular clock and makes it difficult to get to bed before midnight. This <a href="https://doi.org/10.1016/j.cell.2017.03.027">inherited “night owl” gene</a> is estimated to be pretty common, found in nearly 1 out of 75 of us. </p>
<p>Understanding the powerful regulation of biology by circadian rhythms is beginning to lead to far-reaching changes in policy. For example, rather than arbitrarily forcing our sleep schedules into routines that require early morning wake times, some researchers are showing that adjusting our schedules to fit our natural rhythms may pay off at work and school. This is particularly true for adolescents, who have <a href="https://doi.org/10.1016/j.smrv.2007.07.005">a natural “night owl” tendancy</a> – <a href="https://theconversation.com/sleepy-teenage-brains-need-school-to-start-later-in-the-morning-82484">delaying school start times</a> by even just one hour can significantly <a href="https://doi.org/10.1111/mbe.12056">improve academic performance</a>.</p>
<p>The science is now far enough along in our understanding of circadian clocks that researchers are working to <a href="https://doi.org/10.1038/srep38479">optimize work and sleep schedules</a> with our biology in mind. And all these policy innovations are built on the foundation of the Nobel Prize-winning research with those tiny fruit flies.</p><img src="https://counter.theconversation.com/content/85061/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Carrie L. Partch receives funding from the National Institutes of Health and the National Science Foundation. </span></em></p>Americans Jeffrey Hall, Michael Rosbash and Michael Young share the 2017 Nobel Prize in Physiology or Medicine for work that explained how our cells keep track of time.Carrie L. Partch, Associate Professor of Physical & Biological Sciences, University of California, Santa CruzLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/817402017-08-09T00:23:03Z2017-08-09T00:23:03ZHow to kill fruit flies, according to a scientist<figure><img src="https://images.theconversation.com/files/180252/original/file-20170728-9675-d7oet.jpg?ixlib=rb-1.1.0&rect=4%2C174%2C3067%2C2129&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">A scourge of kitchens everywhere, _Drosophila melanogaster_ — the common fruit fly — stares down the electron microscope that captured its image.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/portrait-fruit-fly-drosophila-melanogaster-scanning-262057940?src=ZMYzI72Gn6rd81ET-f5JtA-1-7">(Shutterstock)</a></span></figcaption></figure><p>As a <a href="http://theconversation.com/sex-matters-male-bias-in-the-lab-is-bad-science-80715">researcher who works on fruit flies</a>, I often get asked how to get them out of someone’s kitchen. This happens to fly researchers often enough that we sit around fly conferences (these actually exist) and complain about getting asked this question. </p>
<p>Meanwhile, we watch the same fruit flies buzz around our beers instead of discussing pithy and insightful questions about the research that we’re pursuing. </p>
<p>But I get it: Fruit flies are annoying. So, fine, here’s how we get rid of them in my lab: We build a trap. It’s not perfect, but it’s OK.</p>
<p><strong>1.</strong> Take a small jar (we use small canning jars) and pour in cider vinegar to about two centimetres deep.</p>
<p><strong>2.</strong> “Cap” the jar with a funnel. You can use a plastic funnel if you have one, but a makeshift paper one works well. </p>
<p><strong>3.</strong> Tape the funnel in place so there are no gaps for the flies to crawl out.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&rect=0%2C352%2C839%2C874&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&rect=0%2C352%2C839%2C874&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=434&fit=crop&dpr=1 600w, https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=434&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=434&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=545&fit=crop&dpr=1 754w, https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=545&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/180241/original/file-20170728-30401-1wujjup.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=545&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Thomas Merritt, who researches fruit flies, shows you how to kill them.</span>
<span class="attribution"><span class="source">(Thomas Merritt)</span>, <span class="license">Author provided</span></span>
</figcaption>
</figure>
<p>Flies fly in and can’t find their way out. Every day or two, replace the vinegar.</p>
<p>Instead of vinegar, you can also use beer or wine, but I prefer to drink one of these while making the traps.</p>
<p>There is actually a little science behind the trap. Fruit flies — at least <em>Drosophila melanogaster</em>, the most common fly buzzing around your bananas — are attracted to aging fruit, rotting fruit in particular. They lay their eggs there and the larvae hatch and feed on the soft, overripe flesh. </p>
<p>To find that fruit, flies use their sense of smell, what we call their olfactory system. What they are sensing, smelling, are things like acetic acid — the molecule that gives vinegar its pungent punch. So, you could bait your trap with fruit, but vinegar jumps right to the chase and lures them in.</p>
<p>The flies flying around your kitchen likely came from outside. <em>Drosophila melanogaster</em> are originally an African species, but they’ve spread across the globe. We call them a “cosmopolitan” species — they’re found wherever people are.</p>
<h2>Where flies come from and why we research them</h2>
<p>The story of how they’ve adapted to so many different environments (like, for example, the tip of Florida or even northern Ontario, where I live) is an interesting one and a hot topic of <a href="https://www.nature.com/articles/srep42766?WT.feed_name=subjects_evolutionary-genetics">current</a> <a href="https://petrov.stanford.edu/pdfs/Flatt-2016-Molecular_Ecology.pdf">research</a>. The flies that buzz around my fruit bowl, at least in the summer and fall, likely came from a local population. I’ve actually done work on flies we collected from the <a href="https://link.springer.com/article/10.1007/s10528-012-9523-3">composter</a> in my backyard.</p>
<p>Interestingly, the combination of a tropical species, a cool day and a warm house is likely why there seem to be more flies in the fall. As the temperature outside goes down (and even on cool summer nights where I live), the flies come inside where it’s warm. Where do the flies go in the winter? We actually don’t know. We know they can’t freeze and live, so our best guess is they hide away in basements waiting for warm weather. There’s actually a name for this idea. We call it the “Root Cellar Hypothesis.”</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=340&fit=crop&dpr=1 600w, https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=340&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=340&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=428&fit=crop&dpr=1 754w, https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=428&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/180250/original/file-20170728-3400-vsesus.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=428&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">A trap Thomas Merritt made from a plastic cup, a sheet of printer paper, and about a quarter cup of cider vinegar.</span>
<span class="attribution"><span class="source">(Thomas Merritt)</span>, <span class="license">Author provided</span></span>
</figcaption>
</figure>
<p>The second question that I, and every other fly researcher, get asked is: Why flies? Good question. The first answer is: Because they’re small. Seriously. </p>
<p>Much of the research I do involves asking how individuals, or small groups of individuals, are similar and different. Asking this question is best done with thousands of individuals. An average experiment in my lab can involve tens of thousands of flies. Imagine doing this kind of work on zebras. That’s a lot of zebras. It also helps that flies grow quickly, reproduce constantly and are super easy (usually) to keep in the lab. </p>
<p>The second reason why we research flies is because they are strikingly similar to humans — or any other animal on our planet. Because life on Earth shares a common ancestry, we have all evolved in complex and interwoven paths from a common ancestor. We share much of our genetics and almost all of our biochemistry. </p>
<p>Sixty to 80 per cent of genes found in humans are found in flies, and essentially all our biochemistry and metabolism is identical. So when we ask a question using flies, we can <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022039/">answer a question that interests us about humans</a>. </p>
<p>It is this relatedness, and the ease of working with them in the lab, that have led to research on <a href="https://theconversation.com/ode-to-the-fruit-fly-tiny-lab-subject-crucial-to-basic-research-38465">flies</a> being the foundation of no less than <a href="https://blogs.brandeis.edu/flyonthewall/translational-findings-how-fruit-fly-research-has-already-contributed-to-human-health/">four Nobel Prizes</a>.</p>
<p>Ironically, as I type this there is literally a fruit fly — <em>Drosophila melanogaster</em> — walking the lip of my coffee cup. The little devils are everywhere.</p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/-O9K3TdejJs?wmode=transparent&start=13" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Why Fruit Flies Are So Hard To Kill (YouTube/Scientific Insider)</span></figcaption>
</figure><img src="https://counter.theconversation.com/content/81740/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Thomas Merritt receives funding from the Natural Sciences and Engineering Research Council and the Canada Research Chairs Program.</span></em></p>How do you rid your kitchen of pesky
fruit flies? A scientist who researches them explains.Thomas Merritt, Professor and Canada Research Chair, Chemistry and Biochemistry, Laurentian UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/590392016-05-16T01:06:35Z2016-05-16T01:06:35ZA ‘sixth sense’ for humidity helps insects stay out of climatic trouble<figure><img src="https://images.theconversation.com/files/122580/original/image-20160515-10679-1deq627.jpg?ixlib=rb-1.1.0&rect=65%2C35%2C954%2C642&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Humidity levels can mean life or death for insects.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/asnalhermite/7296111892">Hasna Lahmini</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc/4.0/">CC BY-NC</a></span></figcaption></figure><p>The amount of water vapor in the air – humidity – profoundly alters our experience of the environment around us. A hot, dry morning in the desert of California feels miles apart from a hot, sticky one in the Cambodian jungle.</p>
<p>People generally dislike hot and humid conditions for good reasons. Our bodies dissipate heat through evaporation of sweat from the skin surface. When humidity is high, this process is less effective, and more blood needs to be pumped to the skin for cooling. This results in fatigue and can ultimately lead to <a href="http://www.cdc.gov/niosh/topics/heatstress/heatrelillness.html">hyperthermia (“heat stroke”)</a>.</p>
<p>Varying levels of humidity characterize all habitats on our planet. Animal species have evolved to tolerate and even to thrive in the most extreme climates, from the frozen tundras of the north to the arid deserts of the equator. It’s particularly impressive that small, cold-blooded animals such as insects can flourish in cold climates as well as in desert habitats. In part, these adaptations are made possible by sophisticated sensory systems that allow them to quickly react to potentially dangerous extremes.</p>
<p>When it comes to air humidity, scientists have known <a href="http://www.jstor.org/stable/1535970?seq=1#page_scan_tab_contents">since the early 1900s</a> that insects possess dedicated sensory systems that detect changes in water vapor in the air. This “sixth sense” for humidity has no direct parallels in big land mammals such as us. But it serves the small critters well as they work to avoid desiccation and to find open water: for example, a pond in which to lay eggs (crucial for many species of mosquitoes). We decided to investigate how these humidity-sensing systems work in insects.</p>
<h2>What’s the neuroscience underlying the system?</h2>
<p>Using our favorite fruit fly <em>Drosophila melanogaster</em> as an experimental subject, we set out to determine just how insects can detect water vapor in the air. Which neurons serve as the humidity sensors in this species? Which genes and receptor mechanisms could be used to detect changes in air humidity? How is the information about external humidity relayed and ultimately processed in the fly’s brain?</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=985&fit=crop&dpr=1 600w, https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=985&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=985&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1238&fit=crop&dpr=1 754w, https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1238&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/122002/original/image-20160510-29544-1l2445u.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1238&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Fly species from different habitats prefer different ranges of humidity. <em>Drosophila melanogaster</em> depicted in Lund, Sweden; <em>D. mojavensis</em> depicted in the Saguaro desert of Arizona; <em>D. teissieri</em> depicted in the afrotropical rain forest.</span>
<span class="attribution"><span class="source">Gallio and Stensmyr</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<p>First, we had to determine the favorite humidity range for our fruit fly. Flies are human commensals – literally “share food at the same table,” in this case invited or not. But though they like to live with us, it turns out fruit flies prefer humidity that is just a touch higher than we do [~70 percent relative humidity (RH) – which, on a hot day, would feel pretty sweaty to us].</p>
<p>We also tested two related fly species that live in different habitats. <em>Drosophila mojavensis</em> lives in the arid deserts of southern California and Mexico, and in our lab tests showed a preference for drier environs. <em>Drosophila teissieri</em> lives in the rainforest, and preferred higher humidity than the two other species. This is an important result: it suggests that humidity preference is finely tuned, reflecting specific adaptations to each species’ habitat.</p>
<p>Next, we used the powerful tools available to fruit fly geneticists to find genes that are essential for this ability to detect and respond to air humidity. In flies, we can turn genes on or off relatively easily via mutation, as well as artificially activating or silencing specific neurons to observe what happens to behavior as a result.</p>
<p>The logic here was simple: if we find genes that, when missing, make the flies insensitive to changes in humidity, we know those genes are normally involved in that sensory system. Once we identify those genes, we can determine where they’re active so we can pinpoint which neurons serve as humidity detectors.</p>
<figure class="align-left zoomable">
<a href="https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=530&fit=crop&dpr=1 600w, https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=530&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=530&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=667&fit=crop&dpr=1 754w, https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=667&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/122004/original/image-20160510-20734-1ts99pe.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=667&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The fruit fly <em>Drosophila</em> detects air humidity through hygroreceptors (green) located in a small sac-like invagination of the antenna.</span>
<span class="attribution"><span class="source">Gallio and Stensmyr</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<p>Long story short, we <a href="http://dx.doi.org/10.1016/j.cub.2016.03.049">identified three related genes</a> without which flies become “blind” to external humidity. Flies missing them show no preference at all for dry or humid air. It turned out that they function within key receptor neurons located in the antenna. They’re found in an unusual little pouch in the back of the antenna called the “sacculus” (literally ‘little sac’) – well-protected from potential water splashes or other dangers. </p>
<p>These humidity detectors – termed “hygroreceptors” from the Greek word for humidity – rapidly respond to a puff of dry air, potentially alerting the animal to the fact that dangerous dry conditions are looming. </p>
<p>Next, we followed the projections of the hygroreceptor neurons into the brain, and discovered they end in a region right next to the one that we’ve previously shown is <a href="http://dx.doi.org/10.1016/j.cell.2011.01.028">targeted by temperature receptors of the antenna</a>. Indeed, in insects, temperature and humidity appear to be detected by distinct receptor systems. But the two will of course interact in the brain to determine how attractive a climate may ultimately be to the fly.</p>
<h2>How evolution and engineers approach humidity</h2>
<p>Discoveries like these reveal some of the clever ways evolution solved basic engineering problems. These solutions are invariably a source of inspiration to human engineers working on related areas. In fact, it is quite interesting to compare how flies measure humidity with how we do it.</p>
<p>Modern hygrometers often rely on changes in the electrical properties of a hygroscopic – “moisture-absorbing” – material. Before the reign of electronics, a number of clever strategies had been used to achieve this same goal. Some of the earliest hygrometers were likely inspired by the common “bad hair day” experience: human and animal hair are strongly hygroscopic and change in shape and length depending on air humidity.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=955&fit=crop&dpr=1 600w, https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=955&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=955&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1200&fit=crop&dpr=1 754w, https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1200&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/122581/original/image-20160515-12583-1s2321y.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1200&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The hair hygrometer, invented by de Saussure in 1783.</span>
</figcaption>
</figure>
<p>Leonardo da Vinci built the <a href="http://www.museoscienza.org/english/leonardo/models/macchina-leo.asp?id_macchina=43">first-ever hygrometer</a> on this principle in 1480. A more sophisticated instrument (that can be <a href="http://www.scientificamerican.com/article/bring-science-home-hair-hygrometer/">easily built as part of a science class</a>) is the famous “hair-hygrometer” invented by the Swiss physicist Horace Bénédict de Saussure in 1783. Here, a single human hair is extended over a pulley that operates a needle, so that changes in the hair’s length can be easily measured to keep track of changes in external humidity.</p>
<p>As it turns out, the fly may use a very similar strategy to measure humidity: the tips of the hygrosensory neurons we discovered are located within tiny hairs (sensilla) in the sacculus. We believe mechanical deformation of these sensilla may ultimately help the fly keep track of humidity levels.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=565&fit=crop&dpr=1 754w, https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=565&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/122583/original/image-20160515-10658-cqekqj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=565&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Freshly hatched <em>Culex</em> mosquito, with swimming larvae in the background.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/canoarias/14875299141">Cano Vääri</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-sa/4.0/">CC BY-NC-SA</a></span>
</figcaption>
</figure>
<h2>Applying hygrometer knowledge in the field</h2>
<p>Understanding how animals sense and respond to key environmental parameters helps us understand how they adapt to their surroundings, and will help us predict what will happen to the distribution and survival of species as the climate changes as a result of global warming.</p>
<p>Moreover, an increasing knowledge of the cogs and gears that pesky insects like mosquitoes use to navigate their environment and find their “prey” suggests new ways to steer them away from us. For instance, researchers are working on <a href="http://www.theatlantic.com/science/archive/2016/01/the-troubled-quest-to-find-a-better-mosquito-repellent/423672/">scrambling the olfactory system of mosquitoes</a>, which they use to locate their blood meals. Our new findings may lead to additional strategies for controlling insect populations, perhaps by leading them away from bodies of water near our cities.</p>
<p><em>We would like to thank the people in our laboratories who conducted most of the work described here: Anders Enjin (catalyst of the collaboration between our two Labs), Emanuela E. Zaharieva, Dominic D. Frank, Suzan Mansourian, as well as our colleague Greg S.B. Suh (NYU) for his contribution.</em></p><img src="https://counter.theconversation.com/content/59039/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Marco Gallio receives funding from NIH and Northwestern University. Previous sources of funding include: HHMI, HFSP, The Wenner-Grens Institute</span></em></p><p class="fine-print"><em><span>Marcus Stensmyr receives funding from The Swedish Research Council and The Crafoord Foundation. </span></em></p>Detecting drier or wetter conditions is crucial for insect survival. We’ve long known they can do this – now researchers have discovered the genetic and neural basis for their humidity-sensing system.Marco Gallio, Assistant Professor of Neurobiology, Northwestern UniversityMarcus Stensmyr, Senior Lecturer of Biology, Lund UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/550492016-02-23T10:07:03Z2016-02-23T10:07:03ZCan organs have a sexual identity?<figure><img src="https://images.theconversation.com/files/112344/original/image-20160222-25891-8s5icu.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Gut feeling.</span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-347021081/stock-photo-human-anatomy-xray-view-of-intestines-showing-stomach-colon-intestines-lungs-urinary-system.html?src=pp-same_artist-347020832--2KCmVG2TmdG6_Je5zzLSw-4">Intestines by Shutterstock</a></span></figcaption></figure><p>A <a href="http://www.nature.com/nature/journal/v530/n7590/full/nature16953.html">new study</a> published in Nature suggests that the stem cells that allow our organs to grow “know” their own sexual identity, and this influences how they function. These findings could explain why the prevalence of some diseases, such as certain cancers, differs between the sexes.</p>
<p>Beyond the obvious reproduction-related anatomical differences between males and females, many other organs also show sex specific characteristics, for example in the form of subtle differences in size or in <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694620/">their susceptibility to disease</a>. The effect of hormones has been extensively researched, and can explain many of the differences. However, less is known about the potential impact of differences between the cells that created the organs themselves.</p>
<p>The researchers found important genetic differences at the cellular level and also demonstrated how these differences impact organ growth, independently of circulating hormones. These findings could shed light on why some diseases prevail in men or women.</p>
<h2>Regenerating gut cells</h2>
<p>To uncover genes that regulate cellular differences between male and female organs, the group, <a href="http://www.miguelaliagalab.com/">led by Irene Miguel-Aliaga</a> studied intestines of fruit flies. Fruit flies <a href="https://theconversation.com/in-praise-of-the-humble-fruit-fly-leading-the-way-on-cancer-research-36628">are good experimental systems</a> to investigate gene function and, importantly, they exhibit clear sex-related traits such as body size (females are larger than males) and <a href="http://elifesciences.org/content/4/e06930v">differences in gut physiology</a>.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/112345/original/image-20160222-25855-1n3pvcj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Fruit fly phenomenon.</span>
<span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-14703085/stock-photo-male-common-fruit-fly-drosophila-melanogaster-sitting-on-a-blade-of-grass-with-green-foliage.html?src=2ouK8sRe7NlZN8BMmMT9FA-1-5">Drosophila melanogaster by Shutterstock</a></span>
</figcaption>
</figure>
<p>The researchers hypothesised that the differences in size and gut physiology between the sexes might be due to intrinsic genetic differences at the cellular level. By monitoring the degree to which different genes were activated in both sexes, the researchers found that subgroups of genes regulating gut function were activated differently in male and female flies. This suggested that “sex-determination” genes (genes that are active due to sex chromosomes) inside gut cells were affecting organ function.</p>
<p>Gut cells are continuously regenerated by gut stem cells through cell division, in which the parent stem cell typically divides into a stem cell plus a specialised cell which will no longer divide but performs functions of the gut. Several mechanisms adjust stem cell divisions to suit the needs of the tissue (for example, if the gut is damaged, stem cells produce more cells to enable tissue regeneration). </p>
<p>By manipulating genes in the cells to act as more “male” or more “female” the authors demonstrated that sex-determinants endowed “female” intestinal stem cells with better ability to divide. This increased stem cell division resulted in longer and better regenerating female guts compared to male guts. Suppressing this “sex-determination path” specifically in intestinal stem cells of a female fly caused the gut to resemble that of a male fly, and activating it in intestinal stem cells of a male caused its gut to increase in size to that of a normal female fly. Further experiments identified additional links between sex-determinants and cell growth, providing a more complete picture.</p>
<h2>Advantages and disadvantages</h2>
<p>Higher rates of cell multiplication can have advantages for an organ, in that it can speed up the rate of repair after injury. In the female flies it improves nutrient absorption to accommodate high nutritional demands linked to reproduction. However, higher proliferation also leads to more rapid ageing, and higher vulnerability to tumours. Consistent with this view, the study showed that female flies were more prone to genetically-induced intestinal tumours than males; moreover, the researchers were able to confirm that suppressing the “feminising genes” reduced the ease with which tumours form in the gut of female fruit flies.</p>
<p>The researchers therefore showed how sex-determining genes in stem cells can control organ function, independently of external hormone influences. This had consequences on organ size and also optimised reproduction in females but came with the risk of increased susceptibility to tumours.</p>
<p>The findings have broad implications in the way we understand tissue maintenance, disease and <a href="http://elifesciences.org/content/5/e10956v1">ageing</a>. Future work will be needed to investigate if the mechanisms discovered in the fruit flies’ intestines are also seen in other tissues, and if they are applicable in mammals. If this is the case (which is considered probable), sex-related differences may affect how cells respond to treatments and so by understanding these differences we might be able to develop more effective therapies.</p><img src="https://counter.theconversation.com/content/55049/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Golnar Kolahgar receives funding from Cancer Research UK and the Wellcome Trust. </span></em></p>Hormones may not be the only thing that determines how your organs act.Golnar Kolahgar, Postdoctoral research associate, University of CambridgeLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/494712016-02-15T04:04:26Z2016-02-15T04:04:26ZHow fruit flies can help keep African scientists at home<figure><img src="https://images.theconversation.com/files/111121/original/image-20160211-29190-158k5gm.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Tiny fruit flies under a microscope are a powerful weapon for science.</span> <span class="attribution"><span class="source">Dr Martha Vicente-Crespo</span></span></figcaption></figure><p>The humble fruit fly is being put to an unusual use in sub-Saharan Africa: it’s being used as bait. Its intended lure? It’s hoped that the tiny creature, whose scientific name is _Drosophila melanogaster, _can stop the exodus of researchers from Africa.</p>
<p>At the moment most of the biomedical research being done in African laboratories is performed using rats. Now a <a href="http://drosafrica.org/home">project</a> called DrosAfrica is underway to promote the use of the fruit fly as a model organism for research into human diseases.</p>
<p>There are several reasons for this. Firstly, rats are far more expensive to keep than fruit flies. As an affordable alternative, the fruit fly requires fewer resources to maintain and not as much expensive preparation for experiments.</p>
<p>Also, as a model system, <em>Drosophila</em> enables researchers to perform sophisticated genetics, live imaging, genome-wide analysis and other state-of-the-art approaches. <a href="http://www.ncbi.nlm.nih.gov/pubmed/25624315"><em>Drosophila</em> research</a> has identified thousands of genes with human equivalents. This has provided key insights into cancer biology, pathology, neurobiology and immunology.</p>
<p><em>Drosophila</em> is a prime model organism with tens of thousands of researchers working on every aspect of their biology. This work is aided by electronic open resources such as <a href="http://flybase.org/">Flybase</a> and stock <a href="http://flystocks.bio.indiana.edu/">centres</a> like the one in Bloomington, Indiana in the US. The centre will send <em>Drosophila</em> to any lab in the world for the cost of shipping. These stock centres are funded by governmental grants enabling 100 000s flies to be kept alive in warehouses. </p>
<p>An entire research unit has been built with a focus on understanding a specific aspect of the fly. The most famous is called <a href="https://www.janelia.org/">Janelia</a> Farm, founded by the Howard Hughes Medical Institute in the US. </p>
<h2>A bigger agenda</h2>
<p>The project that’s using fruit flies as bait for scientists is known as DrosAfrica. It wants to drive the paradigm shift from rats to flies as experimental organisms. To do this, project leaders have organised workshops to share fruit fly techniques with universities and research institutes across sub Saharan Africa.</p>
<p>But there’s more to the work than merely extolling the virtues of fruit flies.</p>
<p>We also try to provide basic equipment such as dissecting microscopes, buffers, slides and antibodies for labelling proteins to facilitate the creation of local research communities. Such strong communities will ultimately be able to provide PhD programmes and research opportunities for African researchers. This will mean students don’t automatically feel they have to emigrate when seeking research opportunities.</p>
<p>Powerful local research programmes will also help to place the continent in the spotlight of international research. This could ultimately lead to a return of expatriates with a strong scientific background.</p>
<h2>Activities organised by DrosAfrica: Past and Future</h2>
<p>During the last three years, DrosAfrica has organised three workshops at the Institute of Biomedical Research <a href="http://shs.kiu.ac.ug/">Kampala International University-Western Campus, Uganda</a>. Two focused exclusively on the use of <em>Drosophila</em> for biomedical research. The other concentrated on image and data analysis techniques. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/107786/original/image-20160111-6981-1akcr6a.JPG?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Attendants and faculty members of the first DrosAfrica workshop ‘Drosophila in Biomedical Research: Affordable AND Impacting!’ (Summer 2013)</span>
</figcaption>
</figure>
<p>The workshops’ participants came from sub-Saharan Africa and included Nigerians, Kenyans, Ugandans and a delegate from South Sudan. They were able to work on several common projects and then networked after the workshops using information and resources on a dedicated website. These interactions planted the seed for developing an African <em>Drosophila</em> research community. At this institute, we’ve been lucky to build on the work that the non-profit organisation <a href="http://trendinafrica.org/">Trend</a> has already done. Their team of volunteer scientists equipped the institute’s lab and introduced insect research models to the local scientists.</p>
<p>In 2016 the project plans to deliver workshops at Kenya’s <a href="http://www.icipe.org/index.php">International Centre of Insect Physiology and Ecology</a>. The team is also visiting Nigeria during the second half of February to pave the way for future research collaborations.</p>
<p>The work done over the past few years has already paid dividends. Alumni from the workshops have presented their work at international scientific conferences and supervised undergraduate, Masters and PhD projects. Undergraduate and MSc candidates have graduated on the basis of their research done on flies. One student has submitted an abstract to the <a href="https://www.asbmb.org/">American Society for Biochemistry and Molecular Biology</a>. </p>
<h2>DrosAfrica vision</h2>
<p>The DrosAfrica project is taking important steps to increase the African contribution to scientific advancement. In the coming years we hope to further boost local research opportunities to promote genuine African research led by African researchers, all of them investigating matters of interest to Africans.</p>
<p>And to think: it all started with a tiny little fruit fly.</p>
<p>*DrosAfrica would like to acknowledge the generosity of Faculty members and sponsors, without whom the workshops described above wouldn’t have been possible. They are:</p>
<p>(<a href="http://www.cambridge-africa.cam.ac.uk/">Cambridge Africa</a>, <a href="http://sayansiixd.blogspot.co.uk/">Sayansi</a>, <a href="http://www.wellcome.ac.uk/">Wellcome Trust</a>, <a href="http://twas.org/">TWAS</a>, <a href="http://shs.kiu.ac.ug/">KIU</a>, <a href="http://www.pem.cam.ac.uk/">Pembroke College-Cambridge</a>, <a href="http://www.joh.cam.ac.uk/">St John’s College-Cambridge</a>, <a href="http://www.emma.cam.ac.uk/">Emmanuel College-Cambridge</a>, <a href="http://www.embo.org/funding-awards/fellowships/short-term-fellowships">EMBO</a>, <a href="https://fruit4science.wordpress.com/about/">Fruit4Science</a>, and very specially to FRS <a href="http://www2.gurdon.cam.ac.uk/%7Ekouzarideslab/">Tony Kouzarides</a>).*</p><img src="https://counter.theconversation.com/content/49471/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Fruit flies aren’t just a remarkable organism for research. They are also central to a project that aims to provide more at-home research opportunities for African scientists.Silvia Muñoz-Descalzo, Lecturer in Biology & Biochemistry; Developmental Biology Theme, University of BathTimothy Weil, Lecturer, Department of Zoology, University of CambridgeLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/384652015-03-30T05:55:15Z2015-03-30T05:55:15ZOde to the fruit fly: tiny lab subject crucial to basic research<figure><img src="https://images.theconversation.com/files/76357/original/image-20150328-16090-539qbj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Decreasing funding for fruit-fly research will hurt people, not flies.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/31031835@N08/14412343468/in/photolist-5Nb7B-hHaJsB-hW5oCj-5yvEJN-o3WH4k-6GAxjj-pSg72t-bpHmpx-5wtva2-hW5nMJ-dt3aSH-inJCit-5yrjT8-dt3gC5-5YTxdF-dx1bDt-dt3c2V-7F4rSm-inJ2Hu-inJ1Yd-inJ4Mh-fs2gTX-of4gy4-od2mdm-nXz2Au-g6516s-7gReVr-5yvEe9-dr9FzR-5yrmya-etGhcN-fsXmjY-fsXmhw-nDXMkr-dr9LK7-5yrmBx-fMdZ2P-exp7So-p9LTYD-oSxy8o-dwv7h6-gwvpmz-45Mj9U-daDjoy-7ULyVX-gwvpoP-9RepFj-pfLzfa-axnovX-imKRT/">John Tann</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span></figcaption></figure><p>The world around us is full of amazing creatures. My favorite is an animal the size of a pinhead, that can fly and land on the ceiling, that stages an elaborate (if not beautiful) courtship ritual, that can learn and remember… I am talking about the humble fruit fly, <em>Drosophila melanogaster</em>. By day, a tiny bug content to live on our food scraps. By night, the superhero that contributes to saving millions of human lives as one of the key model systems of modern biomedical research. </p>
<figure class="align-left zoomable">
<a href="https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=900&fit=crop&dpr=1 600w, https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=900&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=900&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1130&fit=crop&dpr=1 754w, https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1130&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/76177/original/image-20150326-8716-me0at8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1130&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Here I am, ready to answer many of your biological questions.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/alfredoperalta/15355275147">Alfredo Peralta García</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-sa/4.0/">CC BY-NC-SA</a></span>
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</figure>
<p>Fruit flies entered the laboratory almost through the back window a little more than 100 years ago. The excitement was still fresh after rediscovery of <a href="http://www.nature.com/scitable/topicpage/Gregor-Mendel-and-the-Principles-of-Inheritance-593">Gregor Mendel</a>’s work on the genetics of peas in 1900. It was an outlandish notion at the time that Mendel’s simple laws of inheritance could apply even to animals. To test this revolutionary idea, scientists were looking for an animal they could keep easily in the lab and reproduce in large numbers.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=860&fit=crop&dpr=1 600w, https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=860&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=860&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1080&fit=crop&dpr=1 754w, https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1080&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/76382/original/image-20150329-16135-cm1n7u.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1080&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption"><em>Drosophila melanogaster</em> spend much of their time in the lab in tubes like these.</span>
<span class="attribution"><a class="source" href="http://commons.wikimedia.org/wiki/File:Drosophila_melanogaster_lab_cultures.jpg">Trick17</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p><a href="http://www.nature.com/scitable/topicpage/thomas-hunt-morgan-the-fruit-fly-scientist-6579789">Thomas Hunt Morgan</a> struck gold when he decided to use the fruit fly as a model. He and his students pushed this prolific little animal to great success. They furthered Mendel’s work to discover that genes are located on chromosomes, where they are arranged, in Morgan’s words, like “beads on a string” – a breakthrough that was recognized with the Nobel prize in 1933. With the success of Morgan’s “flyroom,” the humble fruit fly was set on its way to becoming one of the leading models in modern biology, contributing vast amounts of knowledge to many areas – including genetics, embryology, cell biology, neuroscience. Additional fly Nobel prizes were awarded in 1946, 1995, 2006 and 2011.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=471&fit=crop&dpr=1 600w, https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=471&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=471&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=592&fit=crop&dpr=1 754w, https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=592&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/76175/original/image-20150326-8725-ymm6ou.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=592&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption"><em>Drosophila</em> salivary gland chromosomes.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/11304375@N07/2993343506">Elissa Lei, PhD, NIH</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<h2>A tiny fly stands in for us in basic research</h2>
<p>If you ask a geneticist, humans are brothers to mice and just first cousins to flies, sharing <a href="http://dx.doi.org/10.1038/420509a">99%</a> and <a href="http://dx.doi.org/10.1534/genetics.114.171785">60%</a> of protein-coding genes, respectively. Our anatomy and physiology are also related, so that we can use these laboratory animals to design powerful experiments, hoping what we find will be of significance to animals and humans alike. It’s undeniable that the research on animal models – such as nematodes, flies, fish and mice – has contributed immensely to what we know about our own body and as a result is helping us tackle the <a href="http://dx.doi.org/10.1124/pr.110.003293">diseases that plague us</a>. On this front, the services of the fruit fly will certainly be required for some time to come.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=465&fit=crop&dpr=1 600w, https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=465&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=465&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=584&fit=crop&dpr=1 754w, https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=584&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/76374/original/image-20150329-16086-bi23sq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=584&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Swarm guys, we’ve got work to do in the lab.</span>
<span class="attribution"><span class="source">Andrew Kuang, Gallio Lab, Northwestern University</span>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span>
</figcaption>
</figure>
<h2>Studying fly brains to understand our own</h2>
<p>A recent renaissance in neuroscience is also bringing the fly to the forefront of our efforts to understand the brain. One of the things we least understand is how our own brain produces our emotions and behavior. Scientists are naturally attracted by the unknown, making this one of the most exciting open frontiers in biology. Perhaps, our brain, the ultimate Narcissus, cannot resist the temptation to study itself. Can the humble fly really contribute to our understanding of how our own brain works?</p>
<p>The fruit fly brain is a miracle of miniaturization. It deals with an incredible flow of sensory information: an obstacle approaching, the enticing smell of overripe banana, a hot windowsill to stay away from, a sexy potential mate. And it does this literally on-the-fly, as the little marvel is computing suitable trajectories around the room. Yet the fly brain is composed of only about 100,000 neurons (compared with nearly 100 billion for human beings) and can fit easily through the eye of the finest needle.</p>
<p>The relatively small number of cells is a key advantage for brain mapping, and large efforts are under way to label, trace and catalog every single neuron in the fly brain. Combine this with the unique wealth of information on the genetics of this little animal, and you will see how we are now able to design incredibly powerful experiments in which we alter the “software” (that is, introduce specific changes in the genome) to create animals with unique and predictable changes in the “hardware” (the brain circuits) to ask questions about brain function.</p>
<p>Following this playbook are recent experiments demonstrating, for example:</p>
<ul>
<li>how <a href="http://dx.doi.org/10.1126/science.1202249">sleep enhances memory formation</a> (yes, even in flies!)</li>
<li>how a few sexually dimorphic neurons in the male fly brain promote <a href="http://dx.doi.org/10.1016/j.cell.2013.11.045">male-vs-male fights</a></li>
<li>how specific <a href="http://dx.doi.org/10.1126/science.1249964">‘moonwalker’ neurons</a> in the brain control backward walking</li>
<li>how the brain processes simple <a href="http://dx.doi.org/10.1038/nature14284">hot and cold stimuli</a> to keep this little animal away from danger (my own area of research)</li>
<li>and many more.</li>
</ul>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=414&fit=crop&dpr=1 600w, https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=414&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=414&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=521&fit=crop&dpr=1 754w, https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=521&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/76377/original/image-20150329-16098-1oeghaj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=521&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Highlighted neural pathways processing temperature information in the fly brain.</span>
<span class="attribution"><span class="source">Marco Gallio, Northwestern University</span>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span>
</figcaption>
</figure>
<p>Of course, we can do these kinds of experiments in a number of animal models. But the unique advantage of the fly is that we can pinpoint every single neuron that’s important for a particular response or behavior, precisely map how they connect to each other and silence or activate each one to figure out how the whole thing works.</p>
<h2>Don’t forget the flies</h2>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/76176/original/image-20150326-8713-gx26r.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">I have so much to give!</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/ajc1/6219492055">AJ Cann</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>Just a few weeks back, Chicago hosted the Genetics Society of America’s annual “<a href="http://www.genetics-gsa.org/drosophila/2015/">fly meeting</a>,” bringing together thousands of fly scientists from around the world. One of the topics discussed was that, in this tough economic climate, funding cuts to public agencies are disproportionately <a href="http://dx.doi.org/10.1534/genetics.114.171785">hurting research on fruit flies</a> in favor of more “translational” approaches – that is, research that has more immediate practical applications.</p>
<p>It’s worth remembering that neither Mendel nor Morgan expected that their work could have a direct impact on medicine. Yet when, hopefully soon, we manage to “cure” cancer – a genetic disease <em>par excellence</em> – they should be among the very first people receiving a thank you note from humanity. </p>
<p>Flies still have a lot to contribute to our understanding of all aspects of biology. As with much basic research, the direct benefits from this work may be around the corner, or may take a little longer to find. It would be a big mistake to curb fruit fly research now that the flies are just getting warmed up to tackle some of the most interesting questions in biology.</p><img src="https://counter.theconversation.com/content/38465/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Marco Gallio receives funding from NIH, and has received support in the past from the following non-profit organizations: the Wenner-Grens Foundation, the Human Frontiers Science Program and the Howard Hughes Medical Institute.</span></em></p>These insects are so much more than just the scourge of fruit bowls everywhere. They’re a key model system for all kinds of research that teaches us about our own brain and body systems.Marco Gallio, Assistant Professor of Neurobiology, Northwestern UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/366282015-03-04T06:26:50Z2015-03-04T06:26:50ZIn praise of the humble fruit fly, leading the way on cancer research<figure><img src="https://images.theconversation.com/files/72617/original/image-20150220-21899-tfugc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">You and me have quite a few genes in common. </span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/11304375@N07/2993341786/in/photolist-5yvEe9-5yrmya-5yrmBx-5yvEJN-5yvEoq-5yrkbr-5yvVjh-fKPFbD-5yrjT8-fKPHVD-5AeogB-fL7gmo-6ZbHLK-fKPGMR-fKPGqr-fL7iE5-fKPEmZ-fL7h8U-fKPDEk-fL7hxJ-98qtJB-7JQZCu-bTRpBn-na3Mpw-nvex2T-nJ8q1r-nHQoFx-nvh9Gh-ne5WzM-notrEJ-fKPHyp-fKPE1D-cj53Xq-avN2Hf-9d4SjA-eLrmk-7GJtDA-bUxZxP-c4pvJQ-ngmLMV-dtE7us-dhCDWx-cvXkLN-de7VXz-dqZYpw-ntiSFt-na3FqC-nrg2oL-nxM49z-nvBMnW">André Karwath</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>Cancer research is a global effort involving millions of people, and the fruit fly <em>Drosophila melanogaster</em> – which has been helping our understanding of the disease for decades – is still illuminating the most fundamental part of this process: the beginning.</p>
<p>When praising the fly as a research organism, I am an interested party. I started working with this insect in 1999, and visitors to our institute rewarded my enthusiasm for <em>Drosophila</em> with the nickname “Spanish fly man”. I find fascinating the capacity of the fly to tell us about how cells use genetic information to interact with each other and make decisions about their behaviour. If cells make wrong decisions it can result in them building the rogue structures we know as tumours. </p>
<p><a href="http://www.ncbi.nlm.nih.gov/pubmed/10908582">More than half</a> the human disease genes have an equivalent in <em>Drosophila</em>. This is why <em>Drosophila</em> have been used for over a century to investigate the fundamental mechanisms of inheritance and have turned out to be a great tool for understanding the function of human genes.</p>
<h2>Discussed at highest levels</h2>
<p>In 2008 Sarah Palin, then candidate for US vice-president, <a href="http://www.the-scientist.com/?articles.view/articleNo/26868/title/Palin-vs--the-flies/">dismissed research in fruit flies</a> as “having little or nothing to do with the public good”, contrasting it with the need to spend tax money on research on cognitive disorders. Some of these disorders, however, are being successfully modelled in <em>Drosophila</em>. As recently as last February, US senator Rand Paul <a href="http://www.factcheck.org/2015/02/paul-knocks-flies-and-nih-funding/">used fly research into sex and the ageing process</a> to attack funding decisions at the US National Institutes of Health.</p>
<p>Both Palin’s and Paul’s comments were embarrassingly misinformed, which earned rather vitriolic responses from the media, but highlight how easy it can be to under-appreciate the research power of the fruit fly.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=418&fit=crop&dpr=1 600w, https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=418&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=418&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=526&fit=crop&dpr=1 754w, https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=526&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/73474/original/image-20150302-15950-1sfnom9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=526&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Flies and ageing.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/25484844@N02/2975230865/in/photolist-5wUQtT-fszDb-4ZAJH1-M562z-8nu14s-4KjyJT-bVZvvL-9Lx3M9-M55XB-a4erRt-eZEMry-eZEMmy-eZEMe1-eZtpJe-eZtpfe-eZELaJ-eZEKLA-qsxWhZ-8CRnJE-uZTop-nY7Mpi-7jj9ZF-66ehtE-98EQ1i-7N6wBC-ftqE1w-pakYjP-9Lugva-bn55JM-bn54i4-9Lx4p3-9Lx5K5-9Lx59f-9LueS8-9Lx3eJ-9Lx2yC-9Lx3Bw-eZtqJK-4Si7fb-67ggbH-ekwiBc-jfmpwK-7P6Xtj-d5FFNQ-d5FFuE-d5FFKj-d5FFzG-d5FFqG-d5FFhQ-d5FFEW">berendbotje54</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>Working with the humble fruit fly is fast and cheap, and allows scientific answers with great detail on virtually any general biological problem. For instance it was when using flies that we learned <a href="http://www.ncbi.nlm.nih.gov/pubmed/17245850">our genes reside in the chromosomes</a> in <a href="http://onlinelibrary.wiley.com/doi/10.1002/jez.1400140104/abstract">linear order</a>, and that <a href="http://www.ncbi.nlm.nih.gov/pubmed/17802387">ionising radiation can cause mutations</a>.</p>
<p><em>Drosophila</em> researchers work across a whole range of areas, from stem cell biology to neurobiology, genomics, cancer, evolution, ecology, immunity, ageing, metabolism. All areas of obvious economic and societal interest. And since <em>Drosophila</em> was established as a research workhorse around 1910 it has accumulated an important list of contributions, some rewarded with the Nobel Prize in Physiology or Medicine (in 1933, 1946, 1995, 2006 and 2011, for discoveries ranging from embryonic development to the activation of <a href="http://speakingofresearch.com/2011/10/03/nobel-prize-2011-flies-and-mice-take-a-bow/">the innate immune response</a> to fight infections).</p>
<h2>Genes and cancer</h2>
<p>The fly contributions to cancer research started in 1967, with the discovery of the first tumour suppressor gene (genes whose function is to prevent cells from becoming cancerous).</p>
<p><em>Drosophila</em> has been particularly brilliant at the identification of new genes and drosophilists name new genes after the defects observed when the fly lacks their function and similar defective genes in humans have also been similarly named. Malfunctioning of the hedgehog or porcupine genes – named after fly maggots with an excessive number of spikes in their belly (which allow them to crawl) – and the notch gene (from flies with a serrated wing margin) in humans, are linked to cancers of the blood, breast, intestine, skin or brain.</p>
<p>The molecular similarity between fly and human genes allow studying human disease in <em>Drosophila</em>, sometimes before experimentation in larger animals is required.</p>
<h2>Drug screening</h2>
<p>Genetic similarity also leads to other interesting developments. In the last decade, <em>Drosophila</em> use in human disease research has expanded with the first drug screens in flies. Compared with screening in cells cultured in a dish, fly screens filter out drugs that would have harmful side effects in the whole organism, or are poorly absorbed in the intestine, or degraded during digestion. This saves money in a drug development project.</p>
<p>Of course, <em>Drosophila</em> has important limitations when it comes to learning about human disease: flies lack breasts, a prostate, or lungs (flies breathe through a network of rigid pipes). It is still possible, however, to study the genes associated with human cancers in these and other tissues. </p>
<p>We can breed flies with genetic alterations mimicking those in specific cancers, and then look for an organ in the fly (such as the wing – it does not have to be the “original” human organ) where these alterations lead to cancerous growth, and study how this happens. For instance, working alongside Matt Smalley and Alan Clarke, we are developing models at Cardiff University to study gene functions that we know are important for breast and prostate cancer, but whose functional details are largely unknown, and costly to pursue with research using mice. </p>
<p><em>Drosophila</em> has a long history of research in bio-medicine, and its capabilities as a model are being expanded and updated every year. It is an exciting and fundamental system to work with, that could transform the way research into cancer develops in the future. So after more than a century of use, these humble flies are still at the cutting edge of cancer research.</p><img src="https://counter.theconversation.com/content/36628/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Joaquín de Navascués receives funding from Cardiff University, the Royal Society and the National Centre for the Replacement, Refinement and Reduction of Animals in Research.</span></em></p>Sarah Palin hated them and they’ve helped win Nobel prizes, so what is it about fruit flies that we should value so much?Joaquín de Navascués, Research Fellow in the European Cancer Stem Cell Research Institute, Cardiff UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/373012015-02-09T15:26:32Z2015-02-09T15:26:32ZFruit flies know how to sniff out antioxidants<figure><img src="https://images.theconversation.com/files/71841/original/image-20150212-13203-1ktoaz8.jpg?ixlib=rb-1.1.0&rect=0%2C343%2C2981%2C1512&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The mighty smart fruit fly.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/imortal/3741182834">imortal</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc/4.0/">CC BY-NC</a></span></figcaption></figure><p>The next time you start loading up on food rich in antioxidants at the grocery store, know that you are not alone in the animal world. Other animals such as birds and fruit flies are health conscious too, and make healthy choices about their food. In fact, according to <a href="http://www.sciencedirect.com/science/article/pii/S0960982214015565">new research</a> from the Max Planck Institute of Chemical Ecology in Germany, fruit flies are drawn to rotting bananas by the enticing smell of antioxidants.</p>
<h2>Oxidative stress</h2>
<p>Antioxidants are micro-nutrients, especially present in fruits and vegetables, that help our body to combat harmful oxygen-containing molecules such as free radicals. These free radicals are created daily as a result of normal bodily activities, such as breathing or physical activity, and build up due to stress or lifestyle choices including diet and smoking. Once these free radicals build up, they start to damage proteins, DNA and lipids in our cells. This harmful effect is referred to as “oxidative stress”.</p>
<p>Oxidative stress can damage cells beyond repair, and is a source of inflammation. Humans and mice <a href="https://theconversation.com/immune-cells-react-to-stress-5181">become particularly susceptible</a> to cardiovascular diseases and cancer because of it. Simpler animals like flies die faster on accumulating too much oxidative stress because of cold, eating environmental toxins or being infected by disease-causing microorganisms. </p>
<p>In fact, one of the theories of ageing states that cells and organisms die after piling up oxidative stress. Ramping up antioxidants that neutralise free radicals saves flies from early death. </p>
<p>One way of knowing whether food contains antioxidants is by looking at their colour. Antioxidants such as beta-carotene, lycopene and anthocyanins give fruits and vegetables their typical orange, red or blue colour. And we humans are not the only ones who have noticed this fact. A previous study found that birds like to gorge on fruits rich in antioxidants before going on long flights. They do that by picking out darker fruits that are likely to have more antioxidants.</p>
<p>A <a href="http://www.sciencedirect.com/science/article/pii/S0960982214015565">new study</a> from Max Planck Institute of Chemical Ecology, published in Current Biology, shows that invertebrates such as fruit flies can detect antioxidants by their smell. Not only are these short-lived animals detecting micro-nutrients instead of the regular energy-rich or protein-rich food, but it seems that they are smelling the antioxidants instead of using visual cues in the way that we do.</p>
<p>They found that fruit flies were drawn to rotting bananas because of their antioxidant content. Bananas are rich in a particular kind of antioxidant molecules called hydroxycinnamic acids (HCAs). The family of HCAs contain molecules are also found in other fruits such as blueberries. </p>
<p>Feeding on HCAs helps the fly survive longer if poisoned with a chemical called paraquat. Paraquat kills the flies by generating too much oxidative stress.</p>
<h2>Yeasty goodness</h2>
<p>Bill Hannson, professor of evolutionary neuroethology, and his team found that the fruit flies were not directly drawn by the smell of the HCAs. Fruit fries like to eat rotten fruits with yeast growing on them. The yeast growing on the bananas were converting the HCAs into ethylphenols. The smell of the ethylphenols drew the fruit flies, instead. </p>
<p>Once the fruit flies reach the antioxidant-rich food, they eat more and lay eggs on the fruit. This ensures that their offspring benefit from the antioxidants as well. Along with adult fruit flies, larvae of fruit flies also liked the smell of ethylphenols and were drawn to HCA-rich food.</p>
<p>The researchers identified the specific smell sensing neurons dedicated to smelling the ethylphenols in the nose-like organs of the fruit flies. The organ helps the flies to check the quality of their food and smell other odours. </p>
<p>In recent years, <a href="http://www.the-scientist.com/?articles.view/articleNo/35077/title/Sensing-Calories-Without-Taste/">more and more studies</a> are finding how animals are conscious of their diets, supplementing it with antioxidants. Following these animals could help us understand how early humans found nutritious foods and how that helped us evolve our senses.</p><img src="https://counter.theconversation.com/content/37301/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Anwesha Ghosh does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>The next time you start loading up on food rich in antioxidants at the grocery store, know that you are not alone in the animal world. Other animals such as birds and fruit flies are health conscious too…Anwesha Ghosh, PhD student in Biology, University of RochesterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/321862014-09-29T05:22:23Z2014-09-29T05:22:23ZIf you took #IceBucketChallenge you need to read about these fruit flies<figure><img src="https://images.theconversation.com/files/60164/original/pj7gyq7m-1411720943.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The humble _Drosophila melanogaster_.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/42200412@N03/14858807068">Géry Parent</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span></figcaption></figure><p>If you have a Facebook account, you are likely to have seen someone pour an ice bucket on themselves in the name of raising awareness for amyotropic lateral sclerosis (ALS). ALS is a disease that affects nerve cells in the brain, and it falls into a class of diseases known as neurodegenerative, which include diseases such as Parkinson’s, Alzheimer’s and Huntington’s. All of them are incurable and claim many lives around the world. These diseases can be caused by genetic mutations, but our understanding of what causes these remains poor.</p>
<p>A study, conducted by Manish Jaiswal and colleagues and led by Hugo Bellen and Michael Wangler at the Baylor College of Medicine, just published in <a href="http://www.sciencedirect.com/science/article/pii/S0092867414011131">Cell</a>, takes a key step forward. They identified hundreds of new mutations in specific genes that are associated with various aspects of the development, function and maintenance of neural system in the fruit fly <em>Drosophila melanogaster</em>. The fruit fly is a stand-in for humans, and allows investigation of the molecular mechanisms of 26 human diseases, including ALS.</p>
<p>Researchers could use <em><a href="https://theconversation.com/animals-in-research-drosophila-the-fruit-fly-13571">Drosophila melanogaster</a></em>, because it is a well-established model organism to understand the molecular mechanisms of many human diseases. This is because: about 75% of human disease-causing genes are found in the fly in a similar form, it is easy to work with and breeds quickly, and many tools are available to manipulate any genes in it. </p>
<h2>Messing with a fruit fly</h2>
<p>The standard way of learning about genes is by studying the effect on the fly when a specific gene is “knocked out” from its genome. However, this strategy is sometimes ineffective – for instance, if the gene knocked out is an essential gene required for growth and development, then the fly will not fully grow, rendering the effort useless.</p>
<p>The authors overcame this limitation by inducing mutations in just a few cells in the fly, so that even if an essential gene is mutated, it does not kill the fly during its embryo-to-adult development. The effect of that mutation can be studied by looking at the tissue or organ where that mutation was supposed to act. </p>
<p>This is an important method because it helps to do experiments that can’t be done in humans. For instance, looking at the full genetic data of two siblings suffering from <a href="http://www.nhs.uk/news/2013/08August/Pages/Scientists-grow-mini-human-brain-in-the-lab.aspx">microcephaly</a> – a disease in which size of the head is much smaller than expected – the researchers found that a specific gene, called <em>ANKLE2</em>, was mutated in both. This could be coincidence. But given there are 20,000 genes in the human genome, the chance of such a coincidence are quite low. To find out whether <em>ANKLE2</em> is causing microcephaly, the researchers would need to conduct gene manipulation experiments in humans. Such experiments, however, are unethical.</p>
<h2>Genetic shortcut</h2>
<p>That’s when studying fly and human genetics together becomes crucial. The authors found that flies with mutations in the same gene had small brains too. However, when the human <em>ANKLE2</em> gene was introduced in these mutant flies, they had a normal brain size, providing evidence from the fly that <em>ANKLE2</em> is the culprit. </p>
<p>This technique allowed the authors to isolate 614 new mutations in 165 genes that affect the development, function and maintenance of a functional neural system. But what is perhaps more important is that, these results have helped the authors to suggest a new method for identifying various disease-causing human genes by looking at the mutations in the genomes of patients alongside the mutations in corresponding <em>Drosophila</em> genes. They find that the disease-causing genes in humans have more than one copy of them in the fly, so if one can enlist which genes have more than one copy in the fly, they are likely to be disease-causing in humans. </p>
<p>As more people use this method, we will get closer and closer to finally understanding the genetic basis of many neurological and neurodegenerative diseases.</p><img src="https://counter.theconversation.com/content/32186/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Mohit Kumar Jolly does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>If you have a Facebook account, you are likely to have seen someone pour an ice bucket on themselves in the name of raising awareness for amyotropic lateral sclerosis (ALS). ALS is a disease that affects…Mohit Kumar Jolly, Graduate student in Cancer Systems Biology, Rice UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/296182014-07-25T11:51:09Z2014-07-25T11:51:09ZWhy cold-blooded animals don’t need to wrap up to keep warm<figure><img src="https://images.theconversation.com/files/54900/original/2f4wssjs-1406284877.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Yeah, I'm cool.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/mschmidt62/4180540000">mschmidt62</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-sa/4.0/">CC BY-NC-SA</a></span></figcaption></figure><p>Animals have evolved to occupy almost all corners of the Earth. To survive, no matter the weather outside, they all need temperature-sensitive bodily reactions to work. This is easy for warm-blooded animals, such as humans, because they have the ability to maintain their body temperature. </p>
<p>But cold-blooded animals can’t do that. When the weather changes and the mercury swings one way, their cells get exposed to that change in temperature. Yet cold blooded animals survive just fine. Michael Welte, associate professor of biology at the University of Rochester, may have just discovered how. His team’s findings have been published in the <a href="http://jcb.rupress.org/content/206/2/199.full">Journal of Cell Biology</a>.</p>
<p>At the molecular level, the key to survival is to ensure that proteins are being made at the right time and in the right amount. To do that every cell in the body has an assembly line. This is partly driven by motor proteins, which act like cargo trains delivering the messenger molecule RNA that comes from DNA located in the cell’s nucleus. RNA needs to reach the end of the assembly line where special organelles, called ribosomes, decode the message and make the protein.</p>
<p>“We have found a molecule that keeps protein production balanced when temperatures change,” said Welte. “It happens to do so by controlling cellular transport.”</p>
<p>Theirs was a serendipitous discovery. They were studying fruit flies, which happen to be cold blooded, when they found that making some proteins is difficult for the flies when temperatures change. </p>
<p>As temperatures fall, the protein assembly line slows down more than the cargo trains. This creates an imbalance where, when the motor proteins reach the ribosomes, if the messenger RNA molecules are not used up immediately, they could be lost forever. This could throw the cell completely off-balance, stopping protein synthesis altogether.</p>
<p>But Welte found a special protein, called Klar, that keeps the balance intact. Klar behaves like the emergency brakes of the cargo trains. As soon as the mercury level falls, Klar slows down the motor proteins carrying messenger RNA molecules. Now that the pace of delivery of the blueprints matches the rate of making proteins, the assembly line stays balanced.</p>
<p>In fruit flies, Welte found that the protein assembly line balance is especially important for making a protein called Oskar. Egg cells, from which a fruit fly will hatch, produce Oskar. In the egg cell that still has not decided its orientation, Oskar accumulates and defines where the posterior end will be. The posterior end of the cell will later give rise to the tail after hatching. If Oskar is not made properly that the eggs will not be able to hatch. </p>
<p>When Welte used genetic tools in fruit flies to remove Klar from the cell, he found that losing Klar had no effects on the baby flies that hatched at normal temperature. But as soon as the temperature was lowered, the eggs could not hatch. Development of the fruit fly is completed at colder temperatures only when Klar is present in the egg cell.</p>
<p>Klar is found in all insects in the animal kingdom, where Welte thinks that Klar might be playing a similar role. It would also be interesting to find a similar protein in other cold-blooded animals.</p>
<p>Body temperature in humans does not fluctuate as much as it does in flies. But, with fevers and other conditions, our cells could be exposed to fluctuations in temperature as well. Welte speculates that a similar mechanism could be taking place in our cells as well, keeping our protein production stable. “While we don’t have the Klar protein in our cells, the mechanism for producing proteins is very similar,” Welte said.</p><img src="https://counter.theconversation.com/content/29618/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Anwesha Ghosh does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Animals have evolved to occupy almost all corners of the Earth. To survive, no matter the weather outside, they all need temperature-sensitive bodily reactions to work. This is easy for warm-blooded animals…Anwesha Ghosh, PhD student in Biology, University of RochesterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/192082013-10-18T05:25:55Z2013-10-18T05:25:55ZFly’s brains can tell you a thing or two about your own<figure><img src="https://images.theconversation.com/files/33071/original/zjnxxhyg-1381834050.jpg?ixlib=rb-1.1.0&rect=1%2C0%2C1022%2C683&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Here's looking at you.</span> <span class="attribution"><span class="source">Michael Schmidt</span></span></figcaption></figure><p>You might think you don’t have much in common with a fruit fly. But studying them could tell us more about human conditions such as <a href="http://www.med.upenn.edu/cbir/silent_epidemic.shtml">traumatic brain injury</a> (TBI) - from, for example, a motorbike accident or a blunt hit on the head - which can in some lead many years later to chronic traumatic encephalopathy, an Alzheimer’s-like form of neurodegeneration.</p>
<p>We’ve been studying many aspects of neurobiology in flies: how neurons generate the electrical impulses used in nervous system communication, how they form proper connections (synapses) to relay information from one cell to the next and, more recently, neurodegeneration. We <a href="http://www.ncbi.nlm.nih.gov/pubmed/23613578">recently showed</a> that over-activation of the innate immune response in the brain of flies can lead to neurodegeneration, which is also known to be a consequence of TBI in humans.</p>
<h2>Buzzing around</h2>
<p>It’s not the first time fruit flies have been used to study human disease. Seymour Benzer, one of the great neurogeneticists, <a href="http://oralhistories.library.caltech.edu/27/1/OH_Benzer_S.pdf">was a pioneer</a> of Drosophila neurogenetics - the application of genetic techniques in the Drosophila family of (fruit) flies to study neurobiology and behaviour. </p>
<p>Short-term effects from TBI such as motor incapacitation <a href="http://www.nhs.uk/Conditions/Ataxia/Pages/Introduction.aspx">and ataxia</a> (disorders that affect balance and co-ordination), and long-term effects like the onset of neurodegeneration can be seen in these flies - just as in humans. And flies have already been used as models for <a href="http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=1095&pageNumber=3">Alzheimer’s</a>, <a href="http://www.parkinsons.org.uk/content/project-visit-new-fruit-fly-model-parkinsons">Parkinson’s</a> and Huntington’s diseases. </p>
<p>Concussions and TBI in humans are described mostly in terms of the symptoms. Unlike high blood pressure or diabetes or elevated cholesterol, there is no quantitative readout. This is where Drosophila models are so useful; we can do studies (underway) to look at which genes are activated or inactivated following a brain injury. This not only tells us more about underlying biological mechanisms, but also gives us biomarkers that can reveal the extent and severity of the injury. </p>
<p>We can also reproducibly inflict brain injury to large numbers of flies of a known genetic background. In other words, we can control all the variables so that we can find those changes in gene expression that correlate with the injury.</p>
<h2>You and a fruit fly</h2>
<p>At the level of individual cells, there is no fundamental difference between a nerve cell in a fly brain and a nerve cell in a human brain. Damage to a nerve cell from an impact injury shouldn’t differ in any fundamental way either. </p>
<p>Years of experience have revealed that the basic mechanisms and the genes and molecules that govern these mechanisms are highly conserved between flies and humans, which is now further demonstrated by comparing the <a href="http://1.usa.gov/1bTpJmn">genome sequence of flies</a> and humans.</p>
<p>Flies have already been also used as experimental models for many complex neurobiological mechanisms and neurological disorders. For example, flies have been used as models in studies of sleep, <a href="http://thebrain.mcgill.ca/flash/capsules/histoire_bleu08.html">circadian rhythm</a>, addiction, <a href="http://www.nytimes.com/2012/03/16/health/male-fruit-flies-spurned-by-females-turn-to-alcohol.html?_r=0">alcoholism</a>, epilepsy, learning and memory, <a href="http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=311&pageNumber=5">and neurodegeneration</a>. And much of the information gained from such studies have had direct and important impacts on our understanding of the related mechanisms in humans. </p>
<p>There is every reason (in my opinion) to believe that what we learn about nerve cell injuries in flies will be directly relevant to humans. Human brains are of course more complex, and the particular manifestation of various brain injuries on human activities such as speech, memory and so on are going to be different. But at the level of individual nerve cells the similarities are likely to be far greater than the differences.</p>
<h2>Experimental models</h2>
<p>We need to know much more about TBI. Every person’s brain injury is different and there are so many variables including the type and severity of the injury, the age of the individual and genetic variation among individuals. </p>
<p>But there are limitations to what studies can be performed on people to find out exactly what the immediate and longer term consequence of a particular injury are, which is why we need experimental models. </p>
<p>Existing models mostly use mice and rats. It isn’t that investigators using these models haven’t done many important studies and learned a lot. But there are still inherent limitations to what can be done with rodents because of the numbers you can deal with, the injuries that can be inflicted and the experimental tools that are available. With flies, we can easily control all the variables; we can work with extremely large numbers of individuals and we don’t have to wait months or years to observe long-term outcomes - we can see these after just several weeks. </p>
<p>The hope is that using <a href="http://bit.ly/19KAHac">the experimental tools</a> that we have developed can unravel the underlying cellular and molecular mechanisms behind the short and long-term consequences of TBI. In the best of all possible worlds, an understanding of these mechanisms could help us find a way to treat or even prevent neurodegeneration, in athletes, for example, who may risk knocks to the head. Just as some individuals are more prone to heart disease or cancer or neurodegeneration depending on their genetic background, we’re trying to identify genes in flies that confer either sensitivity or resistance to TBI. It’s early days but there are some indications that genes that confer resistance to TBI are different in younger flies than in older flies.</p>
<p>Drugs that seemed promising in rodents have all failed in clinical trials. The reasons are probably numerous but certainly among them is that we’re dealing with so many variables. We are now in an era of personalised medicine, where we want to find the right drug that works best in a particular individual and differences in genetic makeup are likely to play an extremely important role.</p>
<p>In a word, TBI is complex. Our hope is to get a handle on this complexity using the humble fruit fly.</p><img src="https://counter.theconversation.com/content/19208/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>David Wassarman receives funding from the National Institutes of Health.</span></em></p><p class="fine-print"><em><span>Barry Ganetzky does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>You might think you don’t have much in common with a fruit fly. But studying them could tell us more about human conditions such as traumatic brain injury (TBI) - from, for example, a motorbike accident…Barry Ganetzky, Professor of Genetics, University of Wisconsin-MadisonDavid Wassarman, Professor of Cell and Regenerative Biology , University of Wisconsin-MadisonLicensed as Creative Commons – attribution, no derivatives.