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I've always rather liked ducks, ever since we hand-reared some ducklings back when I was still a school-kid. Mind you, the innocent me of those days didn't know what I know now about the effects of sperm competition and sexual selection on their reproductive organs. (Those of an enquiring mind will learn more - much more! - in this excellent piece by Ed Yong.) I liked them enough to make mallard behaviour the focus of my Honours dissertation, before moving on to swans.

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Ducks were domesticated multiple times by humans perhaps beginning around 4,000 years ago in Egypt, but dated to around 500BC in China (Zhou, Li, Cheng, Fan et al., 2018). Domestic breeds - with the exception of Muscovy ducks - are all derived from the mallard, Anas platyrhynchos. Selection by humans has given rise to quite a range of different phenotypes, with breeds differing most obviously in size and colouration. One of the most striking is the Pekin duck breed (image below), with its white feathers, very large size relative to the ancestral mallard, and its excellent rate of egg production. (Those yummy duck legs in the supermarket chiller are quite likely from Pekin ducks.) These characteristics made the Pekin duck an ideal focus for Shuisheng Hou, Yu Jiang, and their colleagues in their just-published search for the 'fingerprints' of artificial selection in domesticated waterfowl.  (However, as we'll see, their work has wider relevance.)

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The paper is based on a large sequencing exercise: the team carried out whole-genome resequencingA of 40 wild mallards, 36 ducks from 12 different indigenous domesticated breeds in Southern China, and 30 Pekin ducks from three separate populations, plus another 1026 individuals produced by crossing mallards and Pekin ducks.

It seems that in China there were two phases of artificial selection during duck domestication. The first saw the development of the various indigenous domestic breeds, and the second, the specific development of Pekin ducks. There appears to have been a genetic bottleneck at the point where that breed first formed, followed by either quite a bit of genetic drift, or else artificial selection targeting those desirable white feathers and large bodies.

The researchers identified 45 'candidate divergent regions' (CDRs) on the ducks' chromosomes that appear to be related to domestication, some of which were 'markers' for various genes. For example, two CDRs were closely associated with genes involved in reproduction and nervous system activity: bear in mind that the behaviour of domesticated animals differs from that of their wild brethren.

One CDR was used to identify a gene (MITF) involved in the production of melanin. Mutations in this gene result in a loss of pigment, apparently by down-regulating the activity of all other genes downstream of it in the melanin-producing metabolic pathway. Further genomic work led the team to decide that a mutation in MITF is the underlying cause of the striking white plumage of Pekin ducks, one that would have been strongly selected for once it appeared as the down, in particular, is much valued for quilts and padded clothing.

And other CDRs appeared to be associated with a part of the genome linked to body size - traits such as the weight of various body parts & of the body as a whole. Additional genomic work traced this to a 'growth factor' gene (IGF2BP1) that's "consistently expressed in Pekin ducks but ... barely expressed in mallards" from hatching to at least 8 weeks of age. And feeding studies suggested that the Pekin duck form of IGF2BP1 affected both the feed intake of the birds and the efficiency with which they converted food to body mass, resulting in their bigger body size.

This finding has implications beyond the ducks, though: the researchers feel it's likely that

consistent postnatal expression of IGF1BPa in other animals may also enlarge their body size. Therefore, IGF2BP1 is a strong performance target for meat production ... in animals.

And from an evolutionary point of view, it's notable how quickly these genetically-controlled traits - white plumage and larger body size - became fixed by artificial selection in just over 2,500 years of duck domestication.

 

A This technique's also been used in a recently-published study on domestication of cattle in East Asia.

 

Z.Zhou, M.Li, H.Cheng, W.Fan, Z.Yuan, Q.Gao, Y.Xu, Z.Guo, Y.Zhang, J.Hu, H.Liu, D.Liu, W.Chen, Z.Zheng, Y.Jiang, Z.Wen, Y.Liu, H.Chen, M.Xie, Q.Zheng, W.Huang, W.Wang, S.Hou & Y.Jiang (2018) An intercross population study reveals genes associated with body size and plumage colour in ducks. Nature Communications. DOI: 10.1038/s41467-018-04868-4

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I'm starting to gear up for some Schol Bio preparation days in the regions (hi, Hawkes Bay! See you in 4 weeks!) and realised that I haven't written anything specifically focused on those exams for a while. So I thought that putting something together would be a good way to spend a rather wet Sunday. At these days we usually put quite a bit of time into working on answers to the previous year's questions, so in this post let's look at one from the 2015 paper.

In 2015, the examiner based question #1 on a statement by then-Opposition MP Trevor Mallard that he felt that it could be possible to bring moa back to our national parks

... the moa will be a goer, but we're talking 50-100 years out

and expressed a desire to see

small ones that "don't weigh much more than turkeysA ... ones that I could pat on the head rather than ones that are going to bowl us over...

After providing some other contextual material (as is the norm for Scholarship Biology - be aware that you'll need to factor a reasonable amount of reading time into your planning on the day), the examiner asked students to

Analyse the information provided in the resource material and integrate it with your biological knowledgeB to discuss:

  • the evolutionary and ecological factors that contribute to declining population numbers that may result in the extinction of species AND account for the very large increase in the rate of extinction of species in modern times. Use named examples to support your discussion
  • how humans could manipulate the transfer of moa DNA to restore a moa population to the Rimutaka Forest Park AND analyse the biological implications of this. Give your justified opinion on whether the 'moa is a goer'.

There are a number of factors that could feed into a decline in population size. High on most lists would be a reduction in the genetic diversity of the population, something that could be due to genetic drift. If the population is isolated, there would be little or no gene flow due to migration or breeding with individuals from other populations, which would also have a negative impact on genetic diversity and result in the phenomenon of inbreeding depression. (Think of NZ's black robins, as an extreme example.) This is why those managing endangered species such as takahe & kakapo are careful to mix breeding up where possible.

Then, if a species is a specialist, environmental change could pose a problem if the resources the organisms rely on diminish or disappear; they may lack the flexibility to change to others. Specialists are then perhaps more likely to feel the effects of loss of habitat due to climate change or a natural disaster; if they're a non-migratory species then the problem is compounded. Either way, the population sizes of such species are likely to decline. That environmental change can include the arrival of exotic predators, competitors, & diseases - something that's certainly had a significant negative effect on NZ's native fauna & flora. Takahe, for example, have suffered from competition with deer, but were also badly affected by the arrival of stoats. Mustelids, rats, & feral cats kill native birds, reptiles, and insects much faster than the prey species can replace their losses. And chytrid fungus infections pose a threat to amphibian species worldwide, including our own ancient native frogs.

Ultimately their population size may become too small to be sustainable - this is where the concept of 'effective population size' comes into play. If the total size is large, but most individuals are past their normal breeding age, then the effective population size is small. This means that at the population level, reproductive outputs decline. And once death rate exceeds the birth rate, extinction is on the horizon. In addition, in a small, isolated population inbreeding becomes common, and any harmful recessive alleles may be more likely to be expressed. 

It may not be only that species that's affected, either. Removal of one species from an ecosystem can have ramifications for the entire ecosystem - this relates to the concept of a keystone species.

In all of this, we should not forget or underestimate the impact of our own species. Habitat destruction accompanies human settlement, as does the introduction of new species (in NZ, rabbits, possums and pigs along with the deer, rats, cats, dogs, and mustelids). Humans are reasonably efficient predators themselves: it's estimated that moa became extinct here within 200 years of first human arrival. (Research suggests that human arrival & expansion, coupled with climate change, is implicated in megafaunal extinction in Patagonia & elsewhere.)

So, could we bring 'the moa' back? (I really dislike this whole 'the' thing: there were around a dozen different species of moa in NZ, with their own ecological niches.) In theory, yes, we could. It's possible to extract DNA from moa bones, and Massey University researchers used this aDNA to work out how many species of moa once existed here. Mind you, to bring any species of moa back you'd need to ensure you had its full genome!

Then, you'd need to identify a suitable surrogate parent, remove the nuclear DNA from eggs from that host, replace it with your moa DNA, and implant the egg into the surrogate. What would that surrogate be? Perhaps another ratite, such as an emu? Or - if we're going with Mr Mallard's wish for small & manageable moa - perhaps a turkey, given the similarities in size. You'd need to do this multiple times, with the remains of multiple individuals of your target species, and to clone both male and female moa (using the sex chromosomes to identify them), in order to end up with a genetically-variable breeding population. 

Easy to say. But in reality things are likely to be more complex, & more difficult, than that. It's debatable, for example, whether scientists could find a large enough number of P.geranoides individuals to be able to reconstitute that genetically-variable population. In that case, the threats related to inbreeding & genetic drift would still be there, and the species could well spiral back into extinction. 

From an ecological perspective, moa were reasonably large, and each individual would eat a lot of vegetation each day. Given that the Rimutaka Forest probably isn't the same as it was when moa were in their hey-day, would re-introducing moa have a negative effect on the current ecosystem, particularly on the other herbivores? We need to be able to answer that one, to avoid inadvertently causing further changes to the forest community's species composition. 

So, what would be your final opinion? You could argue, along with Mr Mallard, that yes, "the moa is a goer". Remember that you need to justify that opinion: bringing moa species back could help to re-establish the natural biodiversity of ecosystems that human actions have damaged.

Or, you could say - as I would - that no, this isn't a viable proposal. Firstly, as far as I'm aware, birds have yet to be cloned successfully. (There's a list of cloned species, plus a lot more information, at this FDA link.) And secondly, this seems to be a diversion from a more pressing problem: the need to use that money & scientific effort to conserve those ecosystems and species that we currently have.

 

A Mr Mallard was wise to limit the size of the species he wanted resurrected. After all, the giant moa species, Dinornis robustus & D.novaezelandiae, stood over 2m tall & weighed around 250kg. The much smaller Mantell's moa, Pachyornis geranoides, was under 0.5m tall & would have tipped the scales at 20kg ie roughly turkey-sized. Much less alarming, should you meet one in the bush!

B This reminds me that I also need to write something on what the examiner is looking for, in giving an instruction like this.

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Pangolins are strange little creatures, with their diet of ants and termites, and the entire outer surface of their bodies covered with armour-like scales (face, belly & the inner surfaces of the limbs are either hairy or naked). When in danger, pangolins are able to roll up in a ball, presenting only that armoured surface to a predator.

Actually, some of them aren't so little: from nose tip to tail tip, they range from 75 cm to more than 1.5 m in length, with their strong tails making up about half of that. Arboreal species tend to be smaller, just a couple of kilos in weight, but apparently the giant pangolin can weigh in at over 30kg. 

Ground Pangolin at Madikwe Game Reserve

Image by David Brossard (Scaly Anteater exits stage left) [CC BY-SA 2.0 (https://creativecommons.org/licenses/by-sa/2.0)], via Wikimedia Commons

In taxonomic terms pangolins have their own order (Pholidota), with a single family (Manidae) and genus, Manis; there are 4 species in Africa and 4 in Asia. Like giant anteaters they are toothless (edentate), & indeed, they converge with the giant anteaters in a number of ways and for a while the two groups were thought to be closely related. However, it seems that molecular data (from DNA & amino acids) places the pangolins' order as a sister group to the carnivores. So, the toothless state characteristic of both types of anteater has evolved more than once, as has the heavy musculature and massive claws of their forelimbs. 

I hadn't really thought before about how pangolins manage to digest their diets of termites and ants, after licking them up with those sticky, extrusible tongues. (Here's something else I didn't know: a pangolin's tongue is as long as head & body combined ie half their total body/tail length. It's folded back into a throat pouch when not in use, and the animals produce so much sticky saliva that they have to drink frequently.) It turns out that the stomach is rather like a bird's gizzard: its walls are hardened and it contains sand or very small pebbles, which help to grind up those crunchy meals as the muscles in the stomach wall contract and relax.

It seems that yesterday was World Pangolin Day. It would be nice to think that drawing attention to the plight of these strange little creatures would change the fact that they are currently the most trafficked mammal in the world. After all, they range from vulnerable to critically endangered status and are supposedly protected by both national and international legislation. Sadly I think that greed & stupidity will push them over the edge. 

Why? Because, as this article in The Independent says, pangolins are poached on a huge scale 

for their meat, which is considered a delicacy in China and Vietnam, and their scales, which are used as ingredients in traditional Asian medicine. 

Practitioners believe scales are capable of treating a range of ailments including asthma, rheumatism and arthritis.

That defensive habit of rolling up in a ball is useless against poachers, who can just pick the animals up. So, people are prepared to pay a lot of money for the meat and the scales of these creatures, which is where both greed and stupidity come into it.

Greed: well, money talks. In December 2016, Chinese customs made their largest-ever confiscation of scales - a mind-boggling 3.1 tons from an estimated 7,200 pangolins. Their worth: about $US2 million. Research by TRAFFIC, a network that monitors the international wildlife trade, suggests that around 20 tonnes of pangolins, & pangolin parts, are trafficked each year.

And stupidity, because those hugely expensive scales are made of keratin - nothing more and nothing less than the protein that makes up our own hair and nails. People consuming the pangolin's scales might as well chew their own fingernails, for all the good it would do them. I guess they'll have to, when the pangolins (and rhinos, whose horns are keratin too) are gone from the world.

 

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Polyploidy - the duplication of chromosome sets - is relatively common in plants, and can result in the development of new species. (Many modern food crops are polyploids.) It's much less common in animals, although found in some frogs & salamanders (amphibians) & leeches (annelids). 

So it was with a mix of excitement, surprise, & alarm that I read about a triploid crayfish species: excitement, because I hadn't heard about a polyploid crustacean; surprise, because it's a triploid organism; & alarm, because it's an invasive pest across its range.

File:Procambarus fallax forma virginalis.jpg

Image: Wikimedia commons; photo by Zfaulkes

Procambarus virginalis, the marbled crayfish, was first found in Germany in the mid-1990s but is now widespread in Europe & Africa, including Madagascar. In a paper published this month, Frank Lyko & his colleagues reported on their study of the species' genome (Gutekunst, Andriantsoa, Falckenhayn, Hanna et al., 2017). They found that it has 3 copies of each of its 92 chromosomes (276 chromosomes in total), and that all the chromosomes come from the slough crayfish (Procambarus fallax), but from two individuals that weren't closely related. The team suggested that the marbled crayfish originated from a mating between 2 slough crayfish, where one parent contributed a normal, haploid, gamete (one copy of each chromosome) & the other, a diploid gamete with 2 copies of each chromosome, produced by non-disjunction during meiosis. Their genomic analysis pointed to the aquarium trade in Germany as the source of the new species. 

Now, triploid organisms are usually sterile, because they're not able to produce viable gametes via meiosis. (The same would be true of a pentaploid, with 5 copies of every chromosome.) Yet this crayfish has rapidly become an invasive species, & that means it makes lots of baby crayfish. How does it do this? 

By parthenogenesis. That is, this is a clonal species. (The researchers describe the Madagascan population of P.virginalis as "genetically homogeneous and extremely similar to the oldest known stock of marbled crayfish founded in Germany in 1995.)

Every marbled crayfish is female, producing 'apomictic' eggs by mitosis. No sperm necessary. And because every individual is capable of producing eggs and - in this species, a lot of them - in ideal conditions the species' population can grow much faster than that of a sexually-reproducing species. This gives the marbled crayfish quite an advantage over other, competing, species when it's introduced into a new ecosystem, which is why it has been able to expand quickly across Europe & Africa - having likely arrived in these countries via the aquarium trade. And again, because they are parthenogenetic, you need just a single individual to begin a new invasive population. In Madagascar their spread was enhanced by human activity in terms of moving animals around to establish new food populations, the warmer temperatures (compared to those in Europe), and the ready availability of suitable freshwater habitats, and there's concern that endemic crayfish species, and their unique ecosystems, are threatened by the exotic invader.

But there's much more to this story than a tale of an unusual crayfish. I found it fascinating that that understanding how the marbled crayfish genome evolves over time may have applications to cancer research:

The generation of genetic diversity will be shaped by a complex set of factors, including the intrinsic mutability of the genome, environmental mutagens, genetic drift and selective pressure. All these factors are known to play an important role in the evolution of tumour genomes. The analysis of mutations in marbled crayfish populations provides an opportunity to detect the generation, fixation and elimination of genetic changes with particularly high sensitivity and robustness and could therefore disentangle the specific contributions of individual factors. As such, it will be interesting to further explore marbled crayfish as a model system for clonal genome evolution in cancer.

 

J.Gutekunst, R.Andriantsoa, C.Falckenhayn, K.Hanna, W.Stein, J.Rasamy & F.Lyko (2017) Clonal genome evolution and rapid invasive spread of the marbled crayfish. Nature Ecology & Evolution doi:10.1038/s41559-018-0467-9

 

Interested readers will also enjoy this summary of the paper, with commentary from other scientists. 

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EDIT (11 Feb): it seems that the writer of the 'we're eating poison' piece has decided to remove that page from their site. Which I guess is an improvement over the original. However, the good people over at Metabunk provided some useful links to the past, and this site appears to be the source used for the 'poison' post.

No sooner have I written a post about the synergy between FB and blogging then it happens again :) Again, hat-tip to Yvette d'Entremont, who posted a link to an article purporting to tell consumers how to distinguish between GM & 'regular' tomatoes. The writer of that article certainly wears their heart on their sleeve - just look at the title: "We're Eating A Poison!" And they are wrong, wrong, wrong. Even the image at the top of their article is misleading. 

I did leave a polite comment requesting evidence to support their claims. It appears that the owner of the page didn't like it. I am shocked! Shocked, I say!

Anyway. The main reason that they are wrong is that ...

...

... currently there aren't any genetically-engineered tomatoes on the market. 

There used to be one, the "Flavr Savr", which came out with much fanfare in 1994. It had been modified to enhance its shelf life, but apparently was not a commercial success and was withdrawn in 1997. To date, nothing has replaced it, although there's apparently quite a bit of research still going on into e.g. delayed ripening and resistance to pests and environmental stressors.

At this point it's probably worth noting that the tomatoes we grow (or buy) & eat are themselves the result of centuries of modification by conventional selective breeding - and also techniques such as mutagenesis, which are not exactly 'natural'. Nor are they subject to the same controls and rigorous testing required of any GM organism or product, despite the fact that mutagenesis creates much larger genetic changes than today's very precise techniques for genetic engineering (think CRISPR). And yet conventional breeding methods can also cause problems: they led to the withdrawal of some potato varieties in the US & Sweden, because the spuds thus produced contained dangerously high levels of the poisonous compound alpha-solanine.

Then there's that image. 

They'd obviously like us to think that one - perhaps the lushly rich red one to the left? - is natural/organic, and the other, a GMOA. Especially when they ask, "can you tell the difference between a regular tomato and a genetically modified one?" But, as we know, all commercially-available tomatoes are produced by conventional means. Still, I guess they feel that an image speaks a thousand words. (I woudn't want that rich red one in my sandwich though - it looks like a quick route to sogginess.)

And then there's the supposed "mounting evidence that links [GE foods] to toxic & allergic reactions, sick, sterile and dead livestock, and damage to virtually every organ studied in lab animals". Now, at the very least, I'd expect to see links or citations supporting a sweeping statement like that, but the article offers none. (I asked for them, when I made my sin-binned comment.) Anway, on the livestock front, there are now 22 years' worth of data available on stock fed mostly on GMO foods. Back in 2014 Steven NovellaB wrote about a very extensive review study that looked at the first 19 years of information. The animals covered by the various studies reviewed in the paper Novella discussed number in the billions (that is not a typo). It did not identify any problems of the sort listed in the OP that I'm discussing here. (The split between industry-funded & independent research projects into GMOs is roughly 50:50.)

On allergies - apparently the great majority of food-related allergic reactions in the US are caused by antigens from 8 foods: peanuts, tree nuts, milk, eggs, wheat, soy, shellfish, and fish. only GM soybeans are commercially available. There are a number of fairly stringent tests required of those applying to market foods with a GE component, & in New Zealand the results of these tests have to be reviewed by Food Safety Australia NZ. The goal of these safety assessments?

The goal of the safety assessment is not to establish the absolute safety of the GM food but rather to consider whether the GM food is comparable to the conventional counterpart food, i.e., that the GM food has all the benefits and risks normally associated with the conventional food.

So far no food derived from GMOs has been found to cause new allergies.

TL;DR: a scary headline & some scary 'factoids', unsupported by data of any sort. Colour me unimpressed. 

A And in fact, a reverse image seach on google brings up a large number of iterations of this image, including several pages that make it clear that the paler tom of the two is supposedly teh ebil GMO version. They clearly avoid letting the facts get in the way of a good story. 

B Novella has a couple of more recent posts on this subject here and here. The second link makes for fascinating reading. 

 

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Yvonne d'Entremont (aka SciBabe) recently posted an article on 'alternative' foods and health products for pets, in her usual no-holds-barred style. It's always good to see pseudoscience called out for what it is, and in the case of pet-focused quackery it's a message that needs multiple repeats. Why? Because pets are dependent on us, & we have a responsibility to get things right. Homeopathy is not going to clear a dog of tapeworms, and garlic (often advocated as a flea treatment) is actually rather toxic to cats.

As she says

My Buddy is 11 lbs. He’s afraid of the rain. He needs prescription dog food or else crystals build up in his urinary tract and he pisses blood. He and nature don’t coexist very well. Nature really doesn’t give a shit whether Buddy lives or dies. And since I do care, I’m not so sure that we should use nature as a credentialed source of vitality for a small animal who fears common weather phenomena. Most pets aren’t “natural,” they’re domesticated. They live and thrive on our care.

So much like with human health, don’t leave it up to the internet. Bring your questions about your animal’s health to your veterinarian. Keep observing their behavior and any changes to skin, coat, reactions to food, energy levels, and weight. Get them vaccinations and preventative treatment for appropriate things like fleas and heartworm.

At one point, d'Entremont discusses various diet fads for pets, including veganism (for cats, which are obligate carnivores!!!) & raw food diets. One of her links is to a Nature paper on the impact domestication has had on dogs' digestive systems (Axelsson, Ratnakumar, Arendt, Maqbool et al., 2013), which reports on the genomic evidence for adaptation for a diet that contains a lot more starch than dogs' progenitors, wolves, would ever eat.

That adaptation has occurred over at least 10,000 years. Axelsson & his colleagues note that bones found in burials with humans, from an Israeli site that dates back to 12,000 years before present (ybp) could well be the earliest confirmed dog remains. They cite genomic data suggest that canid domestication began in SE Asia, or the Middle East, around 10,000 ybp, but also comment that the evolution of domestic dogs may well have begun in several regions at much the same time.

While we don't know why dogs were domesticated, it's likely that traits enabling cohabitation with humans would have undergone relatively strong selection: Axelsson et al. suggest that these could include behavioural traits such as reduced aggression and changes in abilities related to social interactions, along with morphological features. 

This paper is based on whole-genome sequencing of both wolves and dogs, in order to identify regions of the genome that might have been subject to natural selection as dogs became domesticated. The research team identified 19 regions that contain genes involved in brain functioning, including several that might be involved in behavioural changes.

But they also found 10 genes key to starch digestion & fat metabolism that also appeared to have undergone evolutionary change during domestication. These genes are involved in breaking starch down into maltose (& other smaller molecules), digesting these molecules into glucose, and moving the glucose into the cells that line the intestine. In humans, salivary amylase begins this process in the mouth, but dogs produce only pancreatic amylase - and the team found a marked increase in the number of copies of the gene coding for this form of amylase in dogs, compared to wolves. They also identified mutations in dogs that could enhance the actual uptake of glucose.

They concluded that 

Our results indicate that novel adaptations allowing the early ancestors of modern dogs to thrive on a diet rich in starch, relative to the carnivorous diet of wolves, constituted a crucial step in the early domestication of dogs. 

In other words, dogs are no longer adapted to a wholly-carnivorous diet. But nor are they suited to veganism. Fad diets for pets are not a good idea. 

 

E.Axelsson, A.Ratnakumar, M-L.Arendt, K.Maqbool, M.T.Webster, M.Perloski, O.Liberg, J.M.Arnemo, A.Hedbammar & K.Lindblad-Toh (2013)  The genomic signature of dog domestication reveals adaptation to a starch-rich diet. Nature 495: 360-364. doi:10.1038/nature11837

 

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A recent FB post from Stuff discussed the rising concerns around the evolution of antibiotic-resistant bacteria. (This is something that Siouxsie Wiles has often written about: here and here, for example; her excellent book on the subject is reviewed here.)

Fairly predictably, it didn't take long for the proponents of essential oils to turn up, soon to be joined by the usual antivax folks and those arguing that an 'alkaline' diet is the best cure-all. (They also believe that drinking lemon juice - an acid - is the best way to achieve thisA. It's not, and alkalosis is not a healthy state of being.) However, someone also commented that we should basically allow natural selection to take its course, by removing the "weak and feeble". It's not the first time I've seen this said, but it annoys me every time.

Firstly, because many diseases don't give a damn whether you're fit & healthy, or not. Smallpox was no respecter of health (or social status), for example; nor was the "Spanish flu"B that caused the pandemic towards the end of World War I. In fact, that particular form of influenza had a more severe effect on the young & the healthy. As this article in the Smithsonian says: 

The 1918 pandemic was unusual in that it killed many healthy 20- to 40-year-olds, including millions of World War I soldiers. In contrast, people who die of the flu [these days] are usually under five years old or over 75.

In the US alone, around 670,000 people died; in New Zealand, the toll was around 8,600. Fiji lost 14% of its population in the space of just 16 days.

This article on the Stanford University site adds further, chilling, information: 

The effect of the influenza epidemic was so severe that the average life span in the US was depressed by 10 years. The influenza virus had a profound virulence, with a mortality rate at 2.5% compared to the previous influenza epidemics, which were less than 0.1%. The death rate for 15 to 34-year-olds of influenza and pneumonia were 20 times higher in 1918 than in previous years. 

In some ways, one of the worst aspects of this pandemic is the way that - in the US at least - truth also became a casualty, with public health officials initially lying about its severity and spread. They were supported in this by newspaper editors, who refused to print letters from doctors that warned of the danger. 

What was it that killed so many healthy young people, in particular? The general consensus seems to be that their deaths were largely due to the impact of their own immune systems, which mounted such a strong response that they severely damaged the patients' lungs (which also made it much easier for secondary bacterial infections, such as pneumonia, to take hold). For these people, "weak & feeble" didn't come into it.

The other reason that attitude annoys me is that it betrays a deep misunderstanding of how natural selection operates. This is because the process isn't future-focused. A population under the influence of natural selection may well become better-adapted to its current environment, but what works now may not work so well if the environment should change.

And some genetic traits of which that original commenter might be dismissive, could turn out to be beneficial. After all, the reason that the sickle-cell allele is retained in many African countries is that it offers some protection against malaria (the same is true for thalassaemia in Mediterranean lands), despite the fact that having two copies of this allele (ie being homozygous for it) confers significant, life-threatening disadvantages. 

Then there's cystic fibrosis (CF) - again, in individuals homozygous for the allele, this disorder is life-threatening. But the allele is relatively common: among newborns in Europe, 1 in 2,500 will have CF. It's hypothesised that this is because an individual with a single copy of the allele (a carrier) may be protected from the worst effects of cholera. This is because cholera results in very large amounts of watery diarrhoea, and the same cell-membrane chloride pumps that are implicated in producing all that watery efflux don't work properly in CF individuals. (There's also a suggestion that the allele may have conferred an advantage to some people early in the development of dairying, when lactase persistence was not widespread.)

I guess I shouldn't really read the comments sections!

 

A In fact, there are an awful lot of totally incorrect claims made for the benefits of drinking lemon juice.

B While it's generally been thought that this pandemic strain originated in China, a second Smithsonian story suggests that it may actually have begun in the US, in Kansas, where the virus may have jumped from pigs (possibly pigs already infected with an avian influenza virus).  

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Tomtits and robins were the focus of the first question in the 2016 Schol Bio paper. Specifically, Chatham Island tomtits and robins, which are found only on the Chathams. While at one point they were common and widespread on the islands, the tomtit is classified as nationally endangered, while the black robin is nationally critical & at very high risk of extinction.

The question paper provides two pages of resource materials (maps, photos, and text), and asks students to

Analyse the information provided in the resource materialA and integrate it with your biological knowledge to discuss

  • the reasons why the black robin has a higher risk of extinction than the Chatham Island tomtitB
  • the impact of human intervention on the survival AND evolution of the black robin population.

Compared to the more generalist tomtits, black robins are quite specialised in their habitat and diet. The robins prefer mature forest, with a closed canopy and open understory, while tomits live in mature forest but also venture into shrublands and tussock. This means that the tomtits' options in terms of food and nest sites are less limited. The fact that the robins' poweres of dispersal are limited, so they can't move to suitable habitat on other islands, doesn't help.

One of the fun things about encountering robins in bush on the mainland is that they are ground feeders - you can scuff up some of the leaf litter, step back, and watch them come down to peck through it in search of the invertebrates that they prey on. Tomtits feed at multiple levels in the forest, taking fruit & leaves as well as invertebrate animals. Their more specialised diet means the robins are more at risk following loss of habitat - or a dry year that makes their prey harder to come by. Their ground-feeding habit also means that they're more exposed to predation, something that is also the case for their nesting habits: robins prefer cavities in trees, while tomtit nests are generally quite well concealed (not that this would stop a hungry rat, possum, or mustelid from seeking them out). 

It also takes longer for black robins to replace any losses to predation, let alone grow their population. This is because, compared to tomtits, they have a lower reproductive rate: normally the robins produce one (sometimes two) clutches of 1-4 eggs a year, while tomtits may rear up to three lots of offspring a year, with 3-4 eggs per clutch. (The fact that robins can produce that extra clutch, if the first doesn't survive, was crucial to the efforts to save them when their effective population size was down to a single breeding pair.) The result is that the robins are at greater risk of extinction. 

The fact that the robin population got so low (down to 5 birds in total, with that single breeding pair) means that they went through a severe bottleneck event. As a result of this, and of the subsequent unavoidable inbreeding, there is very little genetic diversity in their population, even though there are now around 250 birds on two islands. This means that the population may not have sufficient variation to allow at least some individuals to survive any significant environmental change. The discovery of birds with deformed beaks, poor bone development, or a distinct lack of feathers has been attributed to that high level of inbreeding.

As the resource information (& a couple of the links above) makes clear, human intervention was the only thing that brought the robins back from the brink and ensured their survival to date. Thus, inducing double clutching, by taking the first clutch and placing the eggs with surrogate parents (first warblers & then, when that wasn't successful because the warblers couldn't provide the right food, tomtits) saw a marked increase in population size. (However, this did come with the risk that the robin chicks would imprint on the wrong parents, something that did actually happen.) Translocating the robins to other islands not only provided suitable habitat and food for the growing population, it also meant that their eggs weren't 'all in one basket': if a predator or disease knocked out the birds on one island, the other could still survive. 

However, conservation workers were pretty much developing their techniques with the robins as they went along, and their interventions did have an impact on the birds' gene pool. I've already mentioned the impact of inbreeding, which can result in increased odds of harmful alleles being expressed. Back in 1984, when someone noticed that a robin had laid her egg on the rim of the nest rather than in the bowl, nudging the egg back into the nest seemed the right thing to do. Unfortunately, by 1989 over 50% of the females were laying rim eggs - the DoC team had inadvertently selected for a dominant, harmful, allele (you can read the original paper here). That is, human action had countered natural selection: normally the egg would have fallen from the nest, or at the least would not have been incubated. Once researchers identified the problem, egg nudging stopped, with the result that natural selection kicked in and the frequency of the allele dropped markedly: now only 9% of females lay eggs on the nest's rim. 

Translocation and fostering could also affect the population's gene pool, and thus its evolution. If there are different selection pressures on the different islands, this could change allele frequencies in the gene pool. And, as previously mentioned, using another species as surrogate parents - while essential at the time - can lead to robins imprinting on the wrong parents and hybridising with them, something that's been confirmed by analysis of microsatellite DNA.

But if it weren't for the dedication and hard work of scientists and conservation workers, the black robin (and many other NZ species) would already have gone the way of the dodo.

 

A I wrote about this in my previous post

B Remember, this question asked students to compare the two species. So a good answer would make that comparison explicit; you shouldn't focus on the robin alone.

 

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Recently, I had an enjoyable chat with Graeme Hill on the subject of sleep. Also on the show was Karyn O'Keeffe, whose research interests are with the physiology of sleep (& the lack of it). My segment focused on the evolution of sleep and yes, I did quite a bit of reading in preparation!

Sleep is mediated by a chemical messenger, melatonin. The onset of darkness triggers the pineal gland to release melatonin, which alters the activity of the neurons in our brains, resulting in sleepiness. Exposure to light destroys melatonin, & so we wake. (Hence the concern about the use of tablets, smartphones etc late into the evening, because of the potential for this to upset the normal sleep-wake cycle.)

One of the things Graeme & I discussed was the evolution of sleep - when did this particular aspect of physiology & behaviour evolve? One of my favourite science writers, Carl Zimmer, wrote about this in 2014. He linked to a study suggesting that sleep may have evolved around 700 million years ago, on the basis of research into gene expression in a marine worm called Platynereis dumerilii.The larvae of these worms move up & down in the water column on a 24-hour cycle (a circadian rhythm), and while the 2-day-old larvae used in the study certainly don't yet have eyes, they do produce and respond to melatonin. Cells on the upper suface of these tiny larvae detect changes in light intensity, and with the onset of darkness, they turn on melatonin production. This stops the beating hairs (cilia) that allow the animals to swim towards the suface, and so they sink slowly down towards the depths. But not so deeply that the light-sensitive cells can't detect dawn's light, which destroys the melatonin and so the larvae swim upwards once again. (Apparently it's even possible to give them jetlag!)

"Well", said Graeme, "why do we sleep? It seems on the face of it a very risky business given the prevalence of nocturnal predators." 

And it's a good question. Why would sleep be selected for, given that you'd think it would make animals more vulnerable to predation? It must have some strong adaptive advantages, to outweigh that risk! Some of the possibilities are canvassed in this short piece in Scientific American, which notes that patterns of sleep and wakefulness vary enormously between species, and also within species depending on time of year - think of hibernation, for example. (Even that varies between species in terms of sleep duration: hummingbirds go into a form of torpor that may last less than a day each time.). The author, Christopher French, suggests that "sleep and related states provide periods of adaptive inactivity" - that is, that a lack of activity can also provide a selective advantage:

Most likely sleep evolved to ensure that species are not active when they are most vulnerable to predation and when their food supply is scarce.

He gives the example of a bat that sleeps around 20 hours a day, rousing to hunt insects that are active in the dusk. Searching for these insects during the day would be fruitless, but would also expose the bats to diurnal predators. But sleep must also be important in some way for the brain, as it's so markedly affected by a prolonged lack of sleep. (And now, I want to know how the melatonin thing works in species like this, that are active at night and sleep during the day. Apparently even nocturnal animals produce the most melatonin at night.)  

A few years back, researchers asked the question, "Is sleep essential?" (Cirelli & Tononi, 2008). (There's an excellent lay summary here - teachers would find it very useful.) I found the paper interesting because, in preparing to test their null hypothesis (that sleep is not essential), the authors first defined sleep:

Sleep is a reversible condition of reduced responsiveness usually associated with immobility.

Most work on sleep has been done in mammals & birds, but it seems that even the humble lab workfly, Drosophila, can be said to sleep: these little flies have periods when they become less responsive to stimuli; if they're forced to stay active, 'sleep pressure' increases; patterns of sleep & wakefulness change with age; hypnotic and stimulant drugs affect their activity; and gene expression in the brain changes with periods of sleep and wakefulness. 

Cirelli & Tononi's paper is open access & well worth reading. They feel that the available evidence doesn't support claims that bullfrogs, for example, do not sleep. Dolphins and other marine mammals, which are constantly moving, still appear to enter a form of sleep - in one hemisphere of the brain at a time - a statement supported by evidence of changes in brain wave activity.

They also discuss the effects of sleep loss - in rats, flies, cockroaches, and humans, prolonged sleep deprivation can ultimately be fatal. (This was the point at which Graeme told me about something called fatal familial insomnia, which sounds awful and is apparently one of the group of prion diseases, along with things like scrapie.) But well before that point, sleep deprivation affects performance, particularly in terms of cognitive performance. So, students take note! an all-nighter or two ahead of major exams is unlikely to work in your favour. 

Cirelli C, Tononi G (2008) Is Sleep Essential? PLoS Biol 6(8): e216. https://doi.org/10.1371/journal.pbio.0060216

 

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I've just come across a most excellent article by the Genetic Literacy Project. In it, Nicholas Staropoli notes that a proportion of the human genome actually has viral origins.

This might sound a bit strange - after all, we tend to think of viruses as our enemies (smallpox, measles, and the human papilloma virus come to mind). But, as Staropoli notes, there are a lot of what are called 'endogenous retroviruses' (ERVs) - or their remains - tucked away in our genome. (An ERV has the ability to write its own genes into the host's DNA.) And he links to a study that draws this conclusion: 

We conservatively estimate that viruses have driven close to 30% of all adaptive amino acid changes in the part of the human proteome conserved within mammals. Our results suggest that viruses are one of the most dominant drivers of evolutionary change across mammalian and human proteomes.

Carl Zimmer writes about one such example in his blog The Loom: it seems that a gene that's crucial in the development of the placenta (that intimate connection between a foetus and its mother) is viral in origin. In fact, one gene encoding the protein syncytin is found in primates - but carnivores have a quite different form of the gene, while rabbits have a different form again, and mice yet another!

This is a very complex evolutionary story indeed. And so you could do much worse than read the two articles, by Staropolis and Zimmer, in their entirety. 

 

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