Open Access Biology Summaries

Elba Room: Surprising Finds in the Partridge Genome

From: “Non-native and hybrid in a changing environment: conservation perspectives for the last Italian red-legged partridge (Alectoris rufa) population with long natural history”, G. Forcina, M. Geurrine, F. Barbanera (2020), Zoology 138

https://doi.org/10.1016/j.zool.2019.125740

Over the past few centuries, it has become ever quicker and easier for people to travel across the world. Advances in sailing, railways and flight have mad the world a much more connected place. But wherever humans go, we tend to bring other organisms with us, whether intentionally (e.g. introducing sheep to New Zealand) or unintentionally (e.g. bringing brown rats into nearly every corner of the planet). This has important implications for health and epidemiology, as we have been seeing in recent weeks, but also for conservation. An area of increasing concern for conservationists is hybridisation between animals that would not normally encounter each other. For example, almost all dingoes have domestic dog ancestry, and there are only a handful of Scottish wildcats left which don’t carry genes from domestic cats. In some cases this sort of genetic ‘introgression’ can help a population adapt to changing circumstances, but it also raises all kinds of broader philosophical questions about whether it is possible or desirable to keep the original organisms ‘pure’. Would we feel the same way about mysterious cats roaming the pine forests of Scotland if we didn’t think they were genetically different from the tabby slinking across your kitchen?

A case in point is the Red-legged Partridge (Alectoris rufa). Once common across Europe, this small hen-like bird has been declining in recent years, and is now listed as a Species of European Conservation Concern. In addition to this, the (possible) Italian subspecies, A. rufa rufa, has been experiencing widespread introgression of genes from the similar Chukar Partridge (Alectoris chukar, a mostly Asian species), as rufa x chukar hybrids released from farms interbred with wild partridge.

To get a clearer picture of the Red-legged Partridge’s genetics, Giovanni Forcina, Monica Guerrini and Filippo Barbanera took genetic samples of partridges from across Elba, a smallish island off the Italian coast. Partridges can fly short distances, but not very well, so the researchers suspected that the Elban partridges may be slightly different to the ones on the mainland.

They found widespread introgression of chukar genes – 57.3% of the partridges across Elba had some mitochondrial DNA (mtDNA, inherited exclusively from the mother) from A. chukar. Interestingly, these birds with part-chukar mothers were particularly common on the eastern side of Elba, where they made up 69.0% of the partridge population. All of the partridges found at one site, Monte Calamita, had chukar ancestry.

This much did not surprise the scientists, given that there had been multiple attempts to introduce Chukar Partridges to Elba in the past. What did surprise them was that a lot of the Elban partridges shared DNA patterns with partridges from Iberia (Spain and Portugal). Indeed, it appears that Spanish and Elban partridges are closely related, as the DNA patterns (haplotypes) exclusively found on Elba were most similar to haplotypes found in Spain, suggesting a very close connection. Spanish partridges were most likely been imported to Elba by private shooting estates in the second half of the 20^th Century to shore up their own partridge populations, but given that there was a significant Spanish presence on the island from at leas the 17^th Century, the authors do not rule out the possibility that Spanish partridges arrived much earlier.

If this study shows one thing, it is that genetics and ancestry are complex, multi-layered things. Genes hitchhiking across the world is nothing new, even if modern technology has made it easier.

How the weather determines a bat’s size

From: “Ambient temperature correlates with geographic variation in body size of least horseshoe bats”, M. Wang, K. Chen, D. Guo, B. Luo, W. Wang, H. Gao, Y. Liu, J. Feng (2020), Current Zoology zoaa004

https://doi.org/10.1093/cz/zoaa004

One of the most interesting and frequently recurring problems in biology is how diversity within species. Under natural selection you’d expect a species to start looking more and more homogenous over time, as the forms best suited to their environment proliferated, but this isn’t always the case. Different sizes, shapes, colours and genes persist within species over very long periods of time. There are a variety of reasons for this. Some alleles (gene variants) are recessive, only affecting individuals with two copies, so they often continue to be inherited regardless of how advantageous or disadvantageous they are. Some genes are helpful, but only if you only have one copy, so individuals with one copy will do well, but not all of their offspring necessarily will (this is known as heterozygote advantage). Some traits are only helpful when they are uncommon, and are selected against as soon as they become common (negative frequency-dependant selection, or NFDS).

But one of the most crucial factors maintaining diversity is that Darwinian fitness is contextual. A trait which is really useful on a mountain might be useless, or worse, by the coast. In some circumstances our theoretical mountaintop and coastal populations may diverge, becoming more and more specialised to mountains or coasts, until they become separate species, but this does not always happen. Often variation is very local, and when animals migrate to a different area their offspring will start to look more like the local population within a few generations.*

One trait that often seems to vary between different geographical areas is size. There are a number of possible explanations, but two seem most likely; either size is determined by the availability of food, or by the temperature. The idea behind the first theory is fairly self-explanatory, but the reasoning behind the second, nicknamed ‘Bergmann’s Rule’, is a little more oblique. It boils down to the fact that small animals lose heat faster. A small animal has a greater proportion of its body near to the outside, losing heat to the air, than a large animal, which can hide its organs underneath many more layers of cells. A small cup of tea cools down faster than a big pot of stew, even when they both start off boiling, simply because proportionately more of the tea is sitting on or near the surface, losing heat to the air. Bergman’s Rule therefore theorises that animals in cold areas will grow slightly bigger, and keep in heat more effectively, while those in hot areas, where the problem is more likely to be having too much heat will grow smaller in order to help them lose heat.

Man Wang’s team wanted to use least horseshoe bats (Rhinolophus pusillus) to test this theory. As fairly small mammals, heat regulation is important to bats – they can only survive by keeping their core body temperature stable (unlike reptiles or amphibians), and they can gain or lose heat from the environment fairly easily, thanks to their thin wings.** As they can fly, they are also able to easily colonise a wide range of different areas with different temperatures. The scientists caught, weighed and measured 246 adult bats from 12 sites across southern China, measuring their mass and head-to-tail body length.

They found quite a lot of variation – the lightest bat weighed 3.10g, with the heaviest weighing over twice that at 6.63g. Variation in length was less dramatic, but still notable – the shortest bat was 29.34mm long, the longest 44.06mm. Size did seem to vary between sites, and, what’s more, did seem to be influenced by temperature. The further north the bats were, the heavier and longer they were. But by far the best predictor of body size was the minimum temperature of the coldest month. The maximum temperature, by contrast, was far less use for explaining variation in weight and length. The authors suggest that there could be three reasons why minimum temperature could be so much more important than maximum temperature. Firstly, bats fly at night, which is usually the coldest part of the day, and so do not experience the hottest temperatures. Secondly, most bats sleep in large roosts in caves and other shelters, which allows them to shelter from heat and the hot sun – caves are colder than the areas just outside them. By staying in the cave or roost, bats can avoid the hottest temperatures. Thirdly, as I mentioned, bat’s wings are extremely good at releasing heat – by positioning their wings, bats can manipulate how quickly they lose heat. The more open the wing, the faster the bat will cool off.

Interestingly, the scientists found that food availability seemed to have little effect on the bat’s size. Hight Primary Productivity, a measure of the amount of vegetation in an area that can be taken as a crude test for the amount of energy available to animals in the area, actually seemed to make the bats smaller. The scientists suggest that this may because in the more productive areas the bats need to store less energy in fat for the winter, as food is more readily available.

Overall, then this does indicate that Bergman’s Rule applies to least horseshoe bats. Bigger bats do better in cold areas, as they lose heat more slowly. The scientists end by pointing out that more studies like this are going to be important in finding out how species are coping with our rapidly changing climate. The climate emergency, as ever, looms on the horizons for all biologists.

* I suspect this is why feral pigeons tend to greyness – brightly coloured tame pigeons interbreeding add all sorts of crazy colour alleles, but selection (specifically, falcons and cats) works in favour of those who blend in – but I’d have to look into it to be sure.

**Which are thin and filled with blood vessels, so lose or gain heat easily – like human ears

Hatching a plan: how modern genetics shed light on an 80-year old theory

From: “Transcriptome of pleuropodia from locust embryos supports that these organs produce enzymes enabling the larva to hatch” B. Koponová, E. Nichberger and A. Crisp (2020), Frontiers in Zoology 17:4

https://doi.org/10.1186/s12983-019-0349-2

When developing inside the egg, many insects develop small organs just below their final pair of legs called pleuropodia. These have been found in all kinds of only distantly related insects, suggesting that it evolved a very long time ago. While this (along with other evidence) suggests that it is likely to have evolved different functions over time in different insects, its main function remains mysterious. Part of the reason for this is that the standard model organism for genetics studies, and one of the most studied organisms in existence, the Drosophila fruit fly, doesn’t have pleuropodia, so the many thousands of scientists working on Drosophila haven’t really had reason to give pleuropodia much thought.*

The main theory about the function of pleuropodia, first proposed by Eleanor Slifer in 1937, is that pleuropodia produce a chemical enzyme which helps the insect hatch by digesting one of the innermost layers of the egg, the serosal cuticle. This derived from Slifer’s observations of grasshopper eggs, which showed the pleuropodia were needed to break down the serosal cuticle – if they were removed, the hatching grasshoppers where stuck inside the egg. Much later, in 1974, two scientists, Novak and Zambre, suggested that it was more likely that the hatching enzyme would be produced by the same epidermal cells that initially laid down the serosal cuticle, on the basis that this was what happened when growing insects shed their skin at later stages of development.** They thought that the pleuropodia instead produced some sort of hormone that triggered the epidermal cells to release a hatching enzyme.

Barbora Konopová, Elisa Buchberger and Alastair Crisp wanted to test these two theories, and see which one worked better. To do so, they looked at what genes were active in the pleuropodia, and what these genes were producing. As genes are ‘expressed’ (activated), they produce transcription RNAs (tRNAs) that are then used to produce proteins from the genes. The more active a gene is, the more tRNAs are produced from that gene. Researchers can measure the amount of tRNAs for each particular gene in in the body, giving a measurement of how active that gene is. This typically varies in different types of cells across the body – in the digestive system, the genes that produce enzymes which digest food will be highly active (‘upregulated’), and the genes that produce muscle will barely be active at all (‘downregulated’). In the muscle tissues, the opposite will be the case – the cells there want to produce muscle, not digest it.

Looking at the pleuropodia of desert locust (Schistocerca gregaria) embryos, Koponová’s team found that when the pleuropodia were active, they expressed (activated) a few different genes that produced chemical enzymes which are able to break down chitin and other proteins that make up the serosal cuticle – supporting Slifer’s original theory that it is the pleuropodia themselves that produce hatching enzymes.*** This theory was further supported by the fact that the scientist’s microscope pictures of the pleuropodia showed them producing secretions as the embryo passed into the yolk. Interestingly, this stopped as the embryo exited the yolk – at the stage of development when Novak and Zambre examined their specimens. Novak and Zambre were not able to find any evidence that the pleuropodia directly affected the serotic cuticle because they were looking at a stage of development after the pleuropodia had ceased to be active. Koponová’s team also found evidence that the pleuropodia had an additional function – they found that genes involved in the immune system were active in the pleuropodia, suggesting it also has some role in protecting the embryo from microbes.

Science is a process of constantly updating and refining ideas as new evidence comes to light, and this study is an excellent example of that, using new evidence to cast light on an eighty-year-old theory.

*Other common model organisms include mice, rats, C. elegans nematode worms and Arabidopsis plants. We also know quite a lot about humans, but you tend to need a pretty good reason before you can experiment on those directly.

**Like snakes, insects must shed their skin to grow, since their skin is too rigid to stretch as they grow.

***The protein chitin is the main chemical that makes up insect cuticles (skin/exoskeleton). Which is why you get Chaurus Chitin when you kill a Chaurus in Skyrim.

Where the Wild Dogs Are: how Kenyan Carnivores decide where to live

From: “What wild dogs want: habitat selection differs across life stages and orders of selection in a wide-ranging carnivore”, H.M.K. O’Neill, S.M. Durant and R. Woodroffe (2020) BMC Zoology 5:1

https://doi.org/10.1186/s40850-019-0050-0

African wild dogs (Lycaon pictus), also known as painted dogs for their bright brown, black and white patterning, are a highly social species of dog found in savannahs across sub-Saharan Africa. An endangered species they, like many other large carnivores, are threatenenenenened by habitat loss and fragmentation, as well as disease and conflict with humans.

As such, it is important for conservationists to know what sorts of habitats wild dogs prefer, in order to preserve and manage national parks and other land for their benefit. Helen O’Neill, Sarah Durant and Rosie Woodroffe set out to investigate this. Moreover, they were also interested to know how what life stage wild dogs were at influenced their preferences, believing that this somewhat understudied question might yield some interesting results.

They looked at data collected between 2011 and 2017 by GPS collars fitted to 18 wild dogs from different packs in Laikipia County, Northern Kenya. The use of different packs is important, as it indicates that their results apply to wild dogs broadly – if they’d followed a single pack, it might be that that particular pack was a particularly eccentric one, which didn’t behave like normal dogs. The scientists also looked at their results by life-stage, according to four classifications: resident non-breeding, resident and heavily pregnant, resident and denning, and dispersing. Resident non-breeding is when a pack stays in roughly the same area, but isn’t currently breeding. Resident and heavily pregnant is when the pack is in the same area, but the alpha female is visibly pregnant. The researchers thought that a pack with heavily pregnant dogs may well adjust its behaviour, but (before this study, anyway) didn’t have any direct evidence for this theory. The third category was resident and denning, where a pack is tied to a small area around their den, due to having very young pups which cannot hunt or travel and need to be kept safe and hidden. This usually means that the packs goes out from the den to hunt twice a day and return soon after. Finally, dispersing is when single-sex groups of young adults, who travel until they find both an opposite-sex group from another pack to form a new pack with (thus reducing inbreeding) and a new home territory.

So what did the researchers find? Across all life stages wild dogs preferred areas with fewer humans and less tree cover – they liked open areas that they could chase antelopes across, away from people and towns. But they also liked to be close to roads and rivers. The ways classed as roads in this study were all main roads, part of Kenya’s road network. Though not motorways, they are still fairly heavily-used and are important links between towns. The researchers suggest that, since much of Laikipia is covered by fairly thick shrubbery, the dogs use the roads and rivers to get around quickly – in other countries, wolves and coyotes have been seen to do similar things.

Though dogs looked for the same sorts of habitat features at all life stages, the strength of their preference seemed to differ between life stage. Denning packs, understandably, had a stronger preference for areas away from humans, and also preferred rockier, more rugged areas on hillsides where they could make dens in relative safety. Packs with heavily pregnant alpha females also avoided humans more, but still stayed close to roads and rivers. The authors do not speculate much on the significance of this, but note that changing behaviour in the weeks leading up to birth, rather than after birth, has been observed in other species, but not studied much at all in wild dogs. I suspect someone may be planning a study into behavioural changes in pregnant wild dogs as I write.

Dispersal groups, by contrast, seemed to spend more time than other groups in areas with more humans, but still, overall, liked to be in areas with lower than average human population density. This suggests that they have to pass through a lot of areas with more humans than they would normally tolerate while travelling. This in itself may explain why they travel so far – they keep going through habitat they don’t want to be in until they find somewhere they do. Which is all any of us can do, really.

Eugenics: good intentions and how to avoid them

Note: I’ve been spending the last week and a half neck-deep in research about eugenics in 19th and 20th Century Britain, so I thought I may as well put my reflections up here. Normal posts resume next week, or this weekend if I have time

In a post-nazi world, eugenics is the dirty secret of western (and a number of eastern) societies. It’s something we describe as an evil to other people, and brush under the carpet when it comes to the things we are proud of – many of the heroes and architects of science, social welfare, statistics, feminism and meritocracy were eugenicists of one sort or another.* From textbook names like Pearson, Fisher, Watson, Crick and Muller to household names like Beveridge, Chamberlain and Churchill, from Fabians to Fascists, eugenics – the ideology that created the death camps – shaped the twentieth century.

So what is eugenics? At its core, it is simply the belief that people can be selectively bred like animals. The theory runs that if people take after their parents, then society and ‘the race’ can be shaped by encouraging people with desirable traits to breed (positive eugenics) or discouraging or preventing people with undesirable traits from breeding (negative eugenics). Like populism and fascism, it is rooted in anxiety about a nation or race ‘degenerating’ in some way, and calls for radical action to arrest this perceived decline. Positive eugenics is usually perceived as milder, and often takes the form of state subsidies aimed at the children of the favoured group. Negative eugenics runs all the way from encouraging or coercing contraception use amongst unfavoured groups through to forced sterilisation and murder. A milder example of negative eugenics might be, say, a cap on the amount of child benefit parents can receive in order to discourage the poorest from having any more than two children, a policy memorably enacted in, er, the UK, less than a decade ago. Eugenics rests on an extreme interpretation of heredity, and assumes that people’s life experiences and environment are of little importance in shaping who they become. The child of a beggar, the theory runs, will inevitably become one themselves, while the child of a parson will be wealthy, intelligent and moral. Therefore, the very poorest, as well as the disabled and ‘mentally deficient’** are unimprovable, and can only be discouraged from existing. As Bishop Barnes put it:

“the genes are genes and master of man’s fate”

Obviously, this view of inheritance has been demolished over and over again by modern science, but it exercised a peculiar power over the elites and middle classes of Britain, America and Europe throughout the 19^th and 20^th centuries. This presents us with a conundrum when considering the legacy of people who we are apt to consider heroes: how did these people, whom we admire for what they did for others, willingly participate in something so evil?

The answer, I think, is that they genuinely thought they were doing the right thing, and the way they thought about ‘the right thing’ should give us some interesting lessons for our own time. Consider the opinion of Havelock Ellis, eugenicist, sexologist and socialist:

“The superficially sympathetic man flings a coin to the beggar; the more deeply sympathetic man builds an almshouse for him so that he need not longer beg; but perhaps the most radically sympathetic of all is the man who arranges that the beggar shall not be born”

This is genuine feeling for the person who is unfortunate enough to have to beg, but to say “it would be better if they had never been born” is one hell of a statement. But this is what lies at the heart of eugenics, telling whole sections of society that it would be better for them and everyone else had they never existed. And for us, the spectre of Hitler cutting out the middleman looms large. I think this is a revealing attitude though, for it rests on several things – a belief that the lives of others have no intrinsic value; a belief that the observer knows better what is best than the subject of their judgement; broadly, a profound lack of both respect and empathy, as well as self-awareness.

Eugenics is an interesting case in that it illustrates a trap that people of every political persuasion fall into: that destroying the lives or wellbeing of people who are part of your country or society is a price worth paying for the improvement of your country or society as a whole. It is a ruthless prioritising of the perceived good of the many over any right of the individual to life or family. Obviously, the challenge of balancing the individual versus the social good is something everyone has to face up to, but in the case of eugenics this is exacerbated by the fact that the sacrifices the ‘unfit’ and ‘undesirable’ were being asked to made were based upon total untruths.

I think this is where the whole scheme really went off the rails. The eugenicist’s faith that the power of science and guided evolution would save the nation or ‘race’ from decline blinded them to the humanity of those they othered and labelled ‘unfit’. This is why eugenics is often called a secular religion or an ideology: the power of the central idea overruled all else for many of its adherents. Like the free marketeer who argues that unemployment benefits distort the labour market, or the communist who argues that a violent revolution must inevitably create utopia, the eugenicist could be found arguing that charity and welfare got in the way of natural selection and caused the nation to degenerate. The pain and death of those who would suffer in the process was an unfortunate inevitability, a small splatter of blood on the foundations of paradise.

So, how do we avoid the pitfalls that eugenics so neatly illustrates? Firstly, I think, we need to listen to those who differ from ourselves. Barely a day goes by when my twitter feed doesn’t fill with the fallout from someone prominent saying something utterly stupid, usually about race, class or gender. This is usually something that a tiny amount of time paying attention to women, BME people, working-class people and social minorities would have told them was problematic – but they, like the eugenicists, were sure that they knew enough not to have to listen to others. There’s not enough listening in this world, and hearing other people’s perspectives not only challenges your own views but reinforces their humanity and makes it more difficult to believe people who are othering and dehumanising them.

That’s the crucial point for me: eugenics spread because people failed to value the humanity of others. As politicians try to divide us, as excitable scientists and tech bros pontificate about wonderful solutions that will forever eradicate disease x or social problem y, we need to remember that every single one of us, no matter what medical conditions or disabilities we have, no matter what ethnicity or gender or political alignment we identify with, no matter how little monetary worth the Great God Market has bestowed upon us, has that indescribable precious spark that is humanity. When eugenicists and their successors start saying that the price of utopia is so many human lives, or preventing so many people from being born, we need to remember that every one of us is precious, and just how high the price of a human life is.

The problem with eugenics is also one of respect and consent. As I’ve discussed, eugenics is predicated on having no respect for the autonomy and humanity of the ‘unfit’. Too often people were sterilised or institutionalised without any attempt to gain their informed consent. Modern medicine views this with horror, but eugenicists had so little respect, so little understanding of the value of the people they were trying to eliminate, that this seemed perfectly sensible to them.

Common sense is dangerous. I’ve studied the slave societies of the 18^th Century, where racism was common sense, and lately I’ve been studying the early 20^th century, when eugenics was common sense. The best thing you can teach yourself to do is question your own assumptions, and to always, always remember how valuable every one of us is. Eugenics illustrates my basic theory about people: most of us want to do the right thing, we’re just not very good at knowing what the right thing is. All we can do is look carefully at the options before us, and remember to choose the option that benefits not just our country as an abstract entity, but benfits all the people living in it.

*for more sophisticated analysis of these areas than I am able to offer, Clare Hanson’s Eugenics, Literature and Culture in Post-war Britain is a good starting point.

**A poorly-defined term under which thousands of predominantly working-class people were imprisoned in institutions for the crime of not living up to middle-class expectations (nominally an IQ of 70 was required to live a normal life, but often inmates did actually score IQs of over 70)

Predicting and preventing the next Zika outbreak

From: “Impact of age-specific immunity on the timing and burden of the next Zika virus outbreak”, M.J. Counotte, C.L. Althaus, N. Low, J. Riou (2019), PLoS Neglected Tropical Diseases 13(12)

https://doi.org/10.1371/journal.pntd.0007978

Zika Virus (ZIKV) is one of several mosquito-borne viruses of the flavivirus family. It was first identified as a distinct from other viruses in 1947 in Uganda. Since then human outbreaks have occurred across the globe, including the famous 2016 outbreak in the Americas. While most people who are infected with the Zika Virus do not show any symptoms, a minority of patients suffer damage to the nervous system. Pregnant women are particularly at risk, as Zika can lead to a number of pregnancy and birth complications, some as severe as miscarriage and, famously, birth defects such as microcephaly in newborns.*

Because of the devastating impact ZIKV can have, it is important for public health officials, particularly in the Americas, to prepare for the next outbreak. Michel Counotte’s team have therefore been working on a mathematical model which they hope will give some kind of indication of when we should expect the next big Zika Virus outbreak. Rather than try to predict a large area, they chose to base their model on existing data collected on Managua, the capital of Nicaragua. This meant that their predictions only hold for Managua, but that is more helpful for the Nicaraguan government than a vaguer prediction covering a wider area! Obviously any model will make a lot of assumptions, several of which may turn out to be wrong, but some idea of what to expect is better than none.

The model predicted a few interesting, and interrelated things. Normally, surviving infection by a virus provides lifelong immunity; the body’s immune system ‘remembers’ it, and can quickly produce the right antibodies to fight it if the virus is encountered again. It is not yet known whether immunity from ZIKV lasts a lifetime or fades away over time. If you assume, as seems likely, that immunity lasts for life, this means that as the people who were not yet born at the last outbreak are at the highest risk. As time goes on, more people are born, and more survivors of the last outbreak die of old age, people who have no immunity make up a larger and larger portion of the population. While most people are immune, the virus has very little chance of causing a serious outbreak – even if one or two people are infected, chances are they won’t infect many other people if nearly everyone around them is immune. This is known as herd immunity, and is why vaccination is so important – as long as most people are vaccinated, epidemics will be prevented. If the numbers of vaccinated people fall below a certain percentage of the population, that’s when problems start.

So, assuming lifelong immunity following Zika Virus infection, the scientist’s model predicts that a sizable outbreak of ZIKV is unlikely to occur in Managua before 2035. But the fact that the immune are aging presents another problem. The most at-risk demographic from a future Zika Virus outbreak is young adults (15-29 years old), simply because those older than them are more likely to already be immune. Unfortunately, 15-29 years old, particularly in Nicaragua, is an age group that also contains a lot of pregnant women: who are in particular danger from Zika Virus.

However, the researchers modelled the impact of a vaccination drive aimed at 15-year old girls between 2021 and 2031. Not only would this significantly reduce the risks facing young women, it would also indirectly reduce the chances of a large-scale outbreak among the general population by prolonging herd immunity. That said, health officials would need to move quickly – the later intervention is left, the less effective it will be, as it will be harder to maintain herd immunity.

There is not yet a vaccine against Zika Virus available – a couple are in trials, but none have yet been conclusively proven effective. What is clear from this study is that as soon as a vaccine is available, public health officials worldwide will have to move fast to protect future generations and prevent future outbreaks.

*As usual, the WHO have a very good overview at https://www.who.int/news-room/fact-sheets/detail/zika-virus Generally, http://www.who.int is my go-to for looking up tropical diseases

If you find an error or lack of clarity in this article, please contact me on j.d.r1612@gmail.com and I’ll fix it as soon as possible

Predicting what a moth sounds like – just by looking

From: “Characteristics of tiger moth (Erebidae: Arctiinae) anti-bat sounds can be predicted from tymbal morphology”, N.J. Dowdy and W.E. Conner (2019) Frontiers in Zoology 16(45)

https://doi.org/10.1186/s12983-019-0345-6

In the 19^th and early 20^th Centuries insect-collecting was a fairly popular hobby amongst well-off ladies and gentlemen with spare time on their hands. When a particularly prolific or eminent collector passed away, their collection would often be donated to a museum, institution or city.* Because of this, many museums worldwide have hundreds of drawers full of Victorian and Edwardian insects from all over the world.** This has been a boon to taxonomists, who can use these collections to compare hard-to-identify specimens with, and to geneticists and evolutionary biologists, who can use DNA samples taken from museum specimens to see how the genetics of these animals has changed over time.

Nicolas Dowdy and William Conner had an idea for another use for these museum specimens. They study tiger moths (Arctiinae), a diverse group of moths which use a specialised ‘tymbal organ’ to produce clicking sounds at pitch which bats can here very well. Many animals use bright colours to signal that they are dangerous or toxic (aposematism)***, but these moths fly at night, when their colours are far less visible. For this reason, many of them produce a high-pitched clicking to signal to any bats looking for a meal not to eat them. Some species of tiger moth do something even odder – they click at a pitch frequency which ‘jams’ bat’s echolocation (sonar), making it very difficult for bats to find them at all. Some tiger moths even use their clicking to locate mates.

Dowdy and Conner’s theory was that if they could understand how the different shapes of the tymbal organs on different moths affected the sound they make, they could begin to predict what the clicks were used for just from looking at museum specimens. To find out more about this, they measured a variety of characteristics of the tymbal organ and the sound it produced across 69 species of tiger moth and tested a variety of mathematical models to see if any of their models could be used to predict anything about the sound the organ produced. They chose to look principally at the click rate (CR) – the largest number of clicks produced by the moth in 100 milliseconds – because this measurement gives both an easy-to-measure indication of the nature of the moth’s sound and also indicates how likely the click is to jam bat echolocation. This is because the click rate needs to be above a certain threshold to have a chance of interfering with a bat’s sonar.

The researchers developed two models that could be used to predict the click rate of a tiger moth. Three characteristics of the moth could be used – the taxonomic ‘family’ (clade) the moth belonged to, the surface area of the moth’s thorax (middle segment), and the number of ‘microtymbals’, tiny little ridges in the tymbal organ which are used to produce the click. Thorax surface area seemed to play a smaller factor, with microtymbal count and clade seeming to be the most important factors determining the click rate.

The scientists are very keen to stress that this is only the first step in researching this problem, and that their models, while they think are very good theories, are still only early-stage theories and will need a lot more development and testing. For example, they couldn’t be sure how well their models work on species with no microtymbals. Most species without microtymbals which they looked at didn’t produce any sound, but some did, usually only producing a single click. The researchers weren’t very sure what the physical differences between these two groups were, or even if the silent moths didn’t just make noises in other situations than the ones they were recorded in.

This is a nice little study, exploring a much-overlooked area, and who knows? Maybe one day soon we’ll be able to know a tiger moth’s click rate just by looking at a museum specimen.

*Yes really. Many museums grew out of city corporations (precursors to modern city councils) needing somewhere to store and display the artefacts which had been donated to them.

**This is also why they often have so many different specimens of the same species – for particularly common or popular species, they got at least one specimen with each collection they received.

***I discussed aposematism in greater depth in this post from November: https://openbiologydigest.home.blog/2019/11/12/seeing-red-why-do-all-these-beetles-look-like-each-other/

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How did malaria get to the Americas?

From: “Plasmodium vivax Malaria Viewed through the Lens of an Eradicated European Strain”, L. van Dorp, P. Gelabert, A. Riuex, M. de Manuel, T. de-Dios, S. Gopalakrishnan, C. Carøe, M. Sandoval-Velasco, R. Fregel, I. Olalde et al (2019), Molecular Biology and Evolution msz264

https://doi.org/10.1093/molbev/msz264

Malaria is, worldwide, a huge danger to human life. It is found across the globe, nowadays mostly in the tropics, although its past distribution is even wider. When you think about it, this is odd. Malaria is caused by a microscopic blood parasite called Plasmodium and transmitted by mosquitoes. So how did it end up in Africa, Asia and, most strangely, the Americas? Mosquitoes have never been particularly able to cross the Atlantic, and humans (we’re pretty confident) first reached the Americas by crossing the Bering Strait – which is rather cold and inhospitable for mosquitoes. Lucy van Dorp and her colleagues have hit upon a discovery which sheds rather a lot of light on this puzzle.

At this point I should clarify that human Malaria can be caused by different species of Plasmodium. Plasmodium falciparum has generally been considered more dangerous, and currently causes 99% of deaths from Malaria worldwide, but Plasmodium vivax is dangerous in its own way, and can cause repeated bouts of sickness from a single infection by hiding dormant inside a person.* Because of this ability to lie low, P. vivax can persist in temperate areas, where cold winters kill off adult mosquitoes, resting until the summer brings back the mosquitoes. Historically, Malaria was found throughout Europe, mostly in marshy areas which provided plenty of stagnant water for mosquitoes to breed in. Malaria is now gone from Europe, largely due to the marshes and fens being drained to make way for agricultural land.** One of the last areas where it persisted was Spain, and microscope slides containing blood samples taken from Malaria patients in the Ebro Delta, Spain between 1942 and 1944 have recently been discovered.

van Dorp’s team were able to extract Plasmodium vivax DNA from these slides, and compare it to samples from all across the modern world. They found that the 1940s Spanish P. vivax is really very similar to the strains currently circulating in South and Central America. When the scientists used the DNA to construct an evolutionary tree (phylogram) of the strains they sampled, they found that the last common ancestor of all the American strains was closer to the Spanish strain than the African and Asian ones. This suggests pretty strongly that the Central and South American strains are descended from if not Spanish, at least from European, P. vivax. Sometime, most likely after regular traffic from Europe to the Americas began in 1492*** it seems that P. vivax travelled across from Europe on ships, possibly Spanish or Portuguese, possibly Dutch or French or British or Italian, settled in America and began to head down its own evolutionary path, gradually become more and more different to the P. vivax of other continents. But that’s not the end of the story. The scientist’s genetic analysis also found a small collection of genes in American P. vivax which were shared with P. vivax from further east – the Indian, Madagascan and Shri Lankan strains. It isn’t the case that P. vivax was deposited by Europeans in the Americas and then isolated from all other strains – traffic across the Pacific seems to have introduced some Indian Ocean P. vivax, which interbred with the American strains, introducing new genes into the American populations. As people move about, bringing other species with them, biological exchanges between continents are not only inevitable, they are also continuous. The evolutionary stories started by humanity are not going to end any time soon, and other organisms will continue to evolve in unexpected ways because of us.

Environmental historians have been interested in the ways Empire and Imperialism affected other species, and particularly diseases, since the 1960s. Empire not only changed human history arguably more than any other process ever, it also changed the natural world.**** Europeans took many different crops from the Americas and left behind horses, cattle, malaria and smallpox (to name just a few examples). The crime of Transatlantic Slavery drew a third continent into the exchange, changing the ecology of each in uncountable numbers of different ways.

Now, advances in genetics are giving us new windows into these processes, and studies like this one are poised to once more revolutionise our understanding of how the ‘natural’ world came to be the way it is. This is certainly a very exciting time to be someone interested in both biology and history!

*The ‘resting’ forms are called hypnozoites.

**Which is also why Lincolnshire, Cambridgeshire, the Netherlands and the Low Countries generally have so much flat farmland.

***I’m well aware that the Icelanders got to America before Columbus, but that didn’t lead to regular transatlantic traffic.

****For a general introduction to this topic, I highly recommend A. Crosby’s The Columbian Exchange. Not every chapter has aged well, but it is still an excellent introduction to the concepts and examples of the field.

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The genes that allow a parasitic worm to infect both rats and snails

From: “The genetic basis of adaptive evolution in parasitic environment from the Angiostrongylus cantonensis genome”, Xu L., Xu M. Xi S., Junyang X., Xin Z., Dai S., Dongjuan Y., Ping H., Weiming H., Yulan Y., Shiqi L., Xiaoying W., Zhongao W. et al (2019), PLoS Neglected Tropical Diseases 13:11

https://doi.org/10.1371/journal.pntd.0007846

Parasites are, when you think about it, incredibly odd. These are entire organisms that have evolved countless specialised adaptations purely to be entirely dependent on leeching* off another organism. Even more strangely, many species change hosts over the course of their lifecycle, and have ridiculously complicated lifecycles. For example the nematode worm (roundworm) Angiostrongylus has seven life stages, including eggs. The first-stage larva** is swallowed by a mollusc (usually a snail of some sort) and spend the next two stages of their life inside the snail. The third stage larva is then able to infect a rodent (most commonly a rat) when the rodent eats the snail. They then migrate to the rat’s brain and develop through two more stages to reach adulthood. As adults they migrate to the lungs, where they reach maturity and breed. The resulting eggs hatch into first stage larva, which migrate to the gut, escape through the rat’s faeces and go in search of snails.

Which, as a lifecycle, is bizarre on many levels.

Lifecycle of *Angiostrongylus cantonensis*, including potenial for human infection, taken from Xu et al 2019.

For one thing, it’s hardly a foolproof plan. Cases of Angiostrongylus accidentally infecting humans are known from across the globe. This can cause a variety of extremely unpleasant and dangerous consequences for the person, including meningitis and brain inflammation (encephalitis). And it’s not ideal for the worm either – humans are a dead-end host that don’t allow it to complete its lifecycle.

There’s also the fact that snails and rats are very different animals with very different biologies. More than that, hosting a parasite is detrimental to both, so both are under fairly strong pressure to evolve effective counter-worm adaptations. Angiostrongylus has to be able to handle two very different environments, both of which are actively hostile to it.

Lian Xu’s team wanted to find out how this affects their genetics. They took a lab strain of an Angiostrongylus species called Angiostrongylus cantonensis and tried to assemble not only its entire genome, but what genes were most active in different stages of its lifecycle. This included when larvae ended up in a host that would not tolerate them, in this case mice. They also gathered pre-existing genetic data from seven other roundworms in order to make comparisons.

In terms of adapting to two different hosts, one particular group of genes stood out. The researchers found eleven different Extracellular Superoxide Dismutase (EC-SOD) genes in two evolutionary clusters, four times more than the other species of roundworm. EC-SOD genes produce an enzyme which provides the first step in making dangerous chemicals known as superoxide radicals safe. Both vertebrates, such as rats, and invertebrates, such as snails, produce a range of toxic reactive oxygen species such as superoxide radicals as a defence against parasites. They are in a low enough dose not to harm the animal producing them, but provide an effective barrier to much smaller animals trying to parasitise them. However, the sheer number of genes that Angiostrongylus cantonensis has which nullify them suggests that A. cantonensis has evolved a response to this defence.

Even more tantalisingly, the first cluster of EC-SOD genes from Angiostrongylus cantonensis were more active in the two life stages where it lives in the rat (or other mammalian host), suggesting they are a specific defence against rat superoxide radicals rather than snail ones.*** In a neat contrast, the second cluster of EC-SOD genes were more active in the third life stage, when the larva lives in the snail. This rather implies that they are specifically aimed against snail superoxide radicals.****

So it appears that Angiostrongylus cantonensis has separate sets of adaptations to protect it against both its hosts – which offers some explanation as to how it is able to routinely infect two such different animals.

Oh, and one other thing – the researchers also found that Angiostrongylus cantonensis had an expanded set of genes for enzymes needed to feed on blood (hematophagy) compared to other nematode roundworms. Which makes sense, as the adults do like to live in arteries. Happy nightmares, dear readers.

*Sometimes literally. [canned laughter]

**larva in this context being a generic term for the early life-stage of any invertebrate

***Interestingly, in A. cantonensis collected from mice (a ‘nonpermissive host’), these genes were less active than in those collected from rats, though what exactly this suggests I’m not altogether sure.

****Or similar chemicals – we can’t assume that all eleven genes are targeted against superoxide radicals as opposed to other reactive oxygen species

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How shelducks decide on their travel plans

From: “Consistent habitat preference underpins the geographically divergent autumn migration of individual Mongolian common shelducks”, F. Meng, X. Wang, N. Batbayer, T. Natsagdorj, B. Davaasuren, I. Damba, L. Cao, and A.D. Fox (2019), Current Zoology 56

https://doi.org/10.1093/cz/zoz056

Common Shelducks (Tadorna tadorna) are a largish species of black, white and brown ducks found across Europe, Asia and Africa. In Britain and a few other areas they are resident year-round, but in many areas they migrate between breeding grounds and (usually coastal) wintering areas. Shelducks which breed in Mongolia migrate to the east coast of China for the winter. As this is a journey of hundreds of miles, they have to stop over at a few different places on the way.

Quack (actually, shelducks don't quack. That's mallards) — Wikipedia’s image of a Shelduck. By DickDaniels (http://carolinabirds.org/) – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=10484193

Fanjuan Meng’s team were interested in where the shelducks stopped over. They took data on the travels of five shelducks from Mongolia which had been fitted with GPS trackers as part of a previous study, and combined it with habitat data taken from remote sensing by satellite. Previous researchers have pored over satellite imagery of various parts of the world, working out ways to classify what sorts of habitat are in an area. Their results provided Meng’s team with an easy way to check what sorts of places the shelducks liked to rest.

The five shelducks took very different routes to the coast, but the patterns of the habitats they chose to stop in were all very similar. Even the different sites visited by the same bird all seemed fairly similar. Every single site the shelducks visited had what the researchers called ‘high water recurrence’. ‘Water recurrence’ is a percentage figure that describes how frequently water returned to the area (this area of northern China and Mongolia has wet and dry seasons). The higher the percentage, the more reliably the site was inundated. This makes sense as shelducks need water to support the aquatic invertebrates they feed on; a reliable food supply makes a big difference when a bird is migrating. They also tended to avoid cultivated land and grassland, presumably as these provided little by way of food or shelter. In the semi-arid regions of Mongolia and Northern China, the researchers suggest that water recurrence was the duck’s overriding concern, as they need reliable water sources to survive the journey.

Different routes shelducks took from Mongolia to the Chinese coast. Taken from Meng et al 2019

Interestingly, there was some suggestion from the scientists’ results that shelducks actually avoided water bodies. Though this seems odd, there is a sensible explanation. In the dry season, many shallow bodies of water dry up, leaving only bare ground. It is quite likely that satellite imaging, possibly taken during the dry season, will have classified these as bare ground, and anything classified as a permanent water body is likely to be large lake or reservoir. Shelducks like shallow water, so will in all likelihood prefer the shallow seasonal lakes which appear in the wet season. Though there’s no way of knowing how much of the land classed as ‘bare ground’ flood during the wet season, the areas that do would have high water recurrence – just the thing the shelducks seem to be looking for.

You can’t generalise very much from five ducks, but this is a clever little study, suggesting very strongly that a migrating shelduck’s highest priority is in choosing which route to take is how reliable the shallow water is. Even though each duck took a different route, each, in its own way, seemed to be bearing that in mind.

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