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Posts Tagged genetics

yes, we have some bananas – just not gm ones (yet) Alison Campbell Mar 09

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Back in 2010 I wrote a post about bananas, following on from a Schol Bio question the previous year. As well as looking at the genotypes of modern bananas, I highlighted the fact that the original wild banana was not a particularly appetising object, with little flesh and a lot of large, hard seeds. Selective breeding for the win!!!

Anyway, it seems like at least one anti-GMO Facebook group has got a case of the vapours about ‘GMO bananas’, this being the only explanation some of its members could think of for the fibres that you’ll often see in the skin of a not-completely-ripe banana when you twist & pull the stalk end. Kevin Folta picked this up in a blog post, noting the lack of knowledge of some of the commenters there (I haven’t quite decided if the one about Morgellon’s is a poe…) – but as Robert Sacerich notes, one of those commenters is giving an object lesson in how NOT to do science communication, & doesn’t help the cause.

And no, we have no GM bananas – at the moment. Sacerich points out that there’s work in progress on developing GM plants that are resistant to the major threats to banana production (Black Sigatoka disease, Banana Bunchy Top virus, and bacterial infections). So such plants may well become a reality in the relatively near future.

But that will have nothing to do with the fibres that so concerned those anti-GMO commenters; they’ve always been with us & were apparently used in cloth production in Japan as early as the 1200s, a practice that’s seen something of a recent resurgence. (I didn’t know that! You learn something new every day.)

rip frank’n'louie, the diprosopic cat Alison Campbell Feb 25

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Seeing this image of a fish with 2 mouths reminded me that I needed to finish writing about Frankenlouie, a janus-headed (diprosopic) cat. It’s funny how the mind works, because the fish definitely isn’t a janus-fish: that would require the mouths to be side-by-side rather than one above the other. (While this is a rather unsightly mutation, the fish seems to have survived in the wild until a fisherman hauled it out.)

Two-mouthed bream

Photo: Garry Warrick)

So – on to Frank’n'Louie.

Frank’n'Louie was (were?) described as a ‘janus cat’ because he had two faces that looked in different directions, like the Roman god Janus (as opposed to that fish, which has two mouths one atop the other). Many people would have found him rather hard to look at, as he had 3 eyes, the middle one of which was blind; two noses; two mouths; and but a single brain. The fact of that single brain means, I suppose, that this really was one, strange-looking, individual cat, rather than the two distinct individuals seen in dicephalic parapagous conjoined twins such as the Hensel sisters. Despite being expected to die soon after birth, Frank’n'Louie attained the ripe old age of 15 years before succumbing to cancer in 2014.

R.I.P.: 'Frankenlouie', the world's oldest Janus cat - a feline with two faces - died at the age of 15 on Thursday, Dec. 4, 2014. The Guinness World Record holder passed away at the Cummings School of Veterinary Medicine at Tuft's University in Grafton, Mass. according to owner Martha "Marty" Stevens of Worcester, Mass. (AP Photo/Worcester Telegram & Gazette, Jim Collins)

Frankenlouie’s features are the result of craniofacial duplication, or diprosopus: an individual with a single body and normal limbs, but a greater or lesser degree of duplication of the face. (He was lucky to survive so long as many janus individuals also have neural tube defects, including – at their most severe - anencephaly, or the absence of a brain, and die very young). When I first saw a picture of this cat I wondered if his features had something to do with conjoined twinning, and apparently that’s often put down as the underlying cause if the organism has two complete faces.

However, another possible cause is a mutation in the gene responsible for the Sonic Hedgehog protein (SHH), which among other roles is involved in the control of craniofacial development. Too much of that protein (overexpression of the mutant form of the gene) results in craniofacial duplication; too little can cause cyclopia, where there is just a single eye. (Infants with cyclopia die soon after birth as the condition is associated with severe brain abnormalities, so the Cyclops of the Ulysses stories would not have been modelled on an actual adult with the condition.)

In fact, SHH plays a crucial role in embryonic development, as this description on the National Institutes of Health gene database makes clear:

It has been implicated as the key inductive signal in patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites.

This means that mutations in the gene coding for SHH can have far-reaching impacts on the development of the brain and nerve cord, limbs, and body segments, while a mutation in one of the enhancer regions (an enhancer is a region on a chromosome that affects transcription of a particular DNA sequence) results in duplication of the thumb.

But there’s more: Sonic Hedgehog is one of a group of ‘evolutionarily conserved’ genes (others in this gene family include ‘Desert Hedgehog’ (!) and Indian Hedgehog) found in vertebrates, so SHH is involved in the patterning of embryo development in all vertebrates, not just in mammals like Frankenlouie. These ‘conserved’ regions of DNA tend to play crucial roles in development and functioning of an organism, and so are relatively unchanged over time: any significant alterations in their sequence, and so in their products, would probably be subject to strong negative selection.  And Sonic Hedgehog’s gene family is in turn related to the hedgehog gene that is involved in proper formation of body segments in Drosophila. So the chromosomal region that’s most likely to be implicated in Frankenlouie’s particular birth defect is one with a very long evolutionary history indeed, one that extends back beyond the split between invertebrate and vertebrate lineages.

food matters aotearoa – an opportunity for real debate? or muddying the waters? Alison Campbell Feb 08

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One of the big stories on my Facebook feed at the moment alerted me to Food Matters Aortearoa and its upcoming Wellington conference. The program for this conference has certainly generated a lot of interest among my friends.

The focus of that interest lies in the line-up of speakers & the agenda of their tour – something my friend & blog-buddy Grant has also written about. The blurb for the Christchurch event pretty much sets the scene: the speakers there (Seralini & Douzelet)

will reveal their experiences with the health problems that chemically grown food can generate

Er, ‘chemically grown food’??? All our food is comprised of chemicals!

But what of the speakers? As Grant notes, Dr Gilles Seralini is perhaps best-known in scientific circles for a now infamous study on the toxicity both of the herbicide Roundup and of maize treated with it. The original paper was retracted but subsequently re-published (seemingly, without any further peer review), without any real attempt to address any of the issues that led to the retraction: the small sample size and the appalling lack of ethical treatment of the study animals (which were allowed to live with extremely large tumours rather than being euthanized at an early stage of tumour development), among others.

Dr Vandana Shiva has done some admirable work around conservation and supporting women farmers in India. However, she has also made some highly questionable claims, including the incorrect but oft-quoted statement that the use of GM cotton led to a marked increase in suicides among Indian farmers. While people may oppose the use of GM technology for a variety of reasons, using demonstrably incorrect information doesn’t bolster their case. There’s an interesting article on Dr Shiva on the New Yorker website, and a discussion on ResearchGate links to a number of valuable resources that look at other claims (for example, the patenting of seeds pre-dates GM technology by some decades).

Similarly, the other major international speaker, Dr Huber, also opposes the use of GM technology & of genetically-modified organisms. I have to say that I continue to be puzzled to the opposition from some quarters to the use of modern genetic modification techniques, while the effects of other tools such as mutation breeding are ignored. Yet the first involves one to a few genes and is well-tested and highly regulated, while the second – which is not regulated in any way – is completely unpredictable and can affect a very large number of gene loci. (A 2008 study found that mutation breeding produced far more genetic change than did transgenesis, & concluded that “the safety assessment of improved plant varieties should be carried out on a case-by-case basis and not simply restricted to foods obtained through genetic engineering.”)

On the face of it, this conference and the associated publicity could offer the opportunity to have some valuable discussion on issues such as the future of agriculture in a time of climbing global population and widespread environmental change, and the safety of GMOs and the various techniques used to produce them. However, since the conference appears to have a strong anti-GMO slant, I doubt this will happen – although I’m prepared to be pleasantly surprised.

 

 

 

 

a surprising misconception Alison Campbell Nov 10

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I spent much of the weekend marking first-year biology exam papers. It was a lovely weekend & I really didn’t want to miss all the nice weather, so I ended up finishing the task well after midnight last night. And in the process I identified evidence of what is, on the surface, a really puzzling misconception, one that relates to the effects of X-chromosome inactivation.

Now, we’d spent quite a while in class discussing X-chromosome inactivation in female mammals: why it happens, how it happens, & its phenotypic effects (anhydrotic ectodermal dysplasia, anyone?). One of the images I used in this discussion was of Venus, a tortoiseshell cat with an extremely unusual colour pattern:

This image comes from the NBC News site, but Venus is a very famous purrball who even has her own Facebook page, and I’ve blogged about her previously. She’s either a chimera, or we’re seeing a most unusual (but not unique) example of the typical X-inactivation tortoiseshell coat pattern. Anyway, I used a similar image of Venus and asked

What is the most likely explanation for the colour pattern shown in the coat of this female cat?

And about 90% of the class answered, “co-dominance”. Which really made me stop & think.

Why? Because it suggests that, while I’m sure they could quote me chapter and verse regarding a definition of co-dominance, they haven’t really thought any further about what that means in phenotypic terms. For if codominance were in play here, with both alleles for coat colour being expressed in each cell where the gene’s active, then we shouldn’t see that clear definition of the two halves of the cat’s face. Instead, both should be a fleckled mix (is ‘fleckled’ a word? Yes, it is; Shakespeare for the win once more) of black & golden hairs (rather like roan coats in cattle & horses).

And this gives me pause – & cause – for thought, because this isn’t a mix-up that I’d have even considered before. Is ‘codominance’ their shorthand for one gene, or the other, being expressed (due to X-inactivation)? Or do they really think that’s how codominance works? If so, it does suggest that a) I didn’t really explain codominance (or X-inactivation) all that well this year, & b) I need to review what I do before teaching that particular session again.

a tale of rare blood groups, or, ‘the man with the golden blood’ Alison Campbell Nov 03

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One of the topics we cover in first-year biology is human blood groups – it’s discussed during genetics classes & also touched on when looking at how immune systems function. I give the genetics classes and, being a regular blood donor myself, thought I knew a bit about at least the common blood groups and their inheritance. But there’s always more to learn, something I was reminded of when I read a fascinating story about people with truly rare blood types: “The man with the golden blood”.

There’s ‘Thomas’, for example: a man who lacks the Rhesus markers completely & so is classified as Rhnull  - in 2010 he was one of an exclusive global club of 43 individuals (of whom only 6 regularly donate their blood). And James, who is ‘Lutheran b negative’, and one of only 550 active donors for this blood type.

This makes known donors precious, in that if someone else with the same group needs a blood transfusion, there are very very few people around the globe who might be able to help them. And helping comes at a cost to the donors, for – as the story tells us – it’s actually easier in many cases to move people across borders than it is to move blood, but because many countries don’t pay donors, then that movement may well be at the donor’s expense. It’s also difficult for people like ‘Thomas’, with his vanishingly rare blood group: his blood can be used by anyone who’s Rhesus negative, but he can receive blood only from another Rhnull person, which means he has to be reasonably careful not to put himself in harm’s way (although he does still go skiing!).

Quite an eye-opener – and a tale I’ll be including in next year’s class.

‘paleo’ diet? or paleofantasy? Alison Campbell Oct 17

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The ‘paleo’ diet story on Campbell Live tonight spurred me to finish my review of one of the most entertaining popular books on genetics that I have read for some time. Entertaining, and informative, in equal measure. I wonder what author Marlene Zuk would have made of the TV story.

book cover Marlene Zuk (2013) Paleofantasy: what evolution really tells us about sex,diet, and how we live.  Norton (New York)

ISBN 978-0-393-34792-0 (paperback)

For in that story we heard gems like this: “It’s a commitment to eating food that is unadulterated, eating food in its most natural state.” Paleo proponents (says the TV story) believe our most natural diet is that of our Palaeolithic cavemen ancestors. Somehow I doubt our ‘cavemen’ ancestors were eating avocados, beetroot, bacon or kale. (There’s also an air of chemophobia, with one proponent of paleo eating stating that their diet contains “[n]othing nasty and nothing you can’t pronounce” – which reminded me of the series of posters by Australian teacher James Kennedy, showing the list of chemical compounds found in natural food items: blueberries, anyone?).

Proponents of the so-called paleo diet seem to think that humans haven’t evolved in the last 10,000 years (since the advent of agriculture), and that this means that our bodies aren’t ‘designed’ to cope with the products of the agricultural revolution. (This, while eating foods that bear little resemblance to their Palaeolithic counterparts. Look at teosinte, the ancestor of maize, for example: small, stone-hard kernels arranged in a few lines on a stalk. Nothing like the fat, soft, juicy kernels on a modern cob of corn.)

As Zuk notes, the paleofantasy happily assumes that at some point in the past (around 10,000 to 40,000 years ago, depending on who you’re listening to), humans were perfectly adapted to their environment, including their diet. But, she asks, why hark back to that particular point in time?

would our cave-dwelling forebears have felt nostalga for the days before they were bipedal, when life was good and the trees were a comfort zone?

Plus, of course, there’s the question of just which ’cavemen’ we’re aspiring to be like. We’ve no guarantee that the life-styles of modern hunter-gatherer populations are a good approximation of life 40,000 years ago. Should we be Inuit, or Kung?

And there’s no reason for us to have stopped adapting to evolutionary pressures once agriculture became the mainstay of human populations – in fact, there’s a great deal of evidence to the contrary, some of which I’ve written about previously -the evolution of lactase tolerance, for example. Similarly, with the spread of arable farming, those with the ability to digest grains would be at an advantage, to the extent that there is a higher number of copies of the gene coding for salivary amylase in populations with a long history of eating starchy grains, compared to populations where the diet has traditionally been low in starches. And Zuk provides many examples of just how rapid evolutionary change can be, in humans and in other animals (changes in cane toad morphology, in the short span of time since their arrival in Australia, are a particularly elegant case in point). The final chapter, which gives considerable detail in answering the question, are we still evolving, would be very useful to biology teachers during human evolution classes.

In other words,

[t]he notion that humans got to a point in evolutionary history when their bodies were somehow in sync with the environment, and that some time later we went astray from those roots – whether because of the advent of agriculture, the invention of the bow and arrow, or the availability of the hamburger – reflects a misunderstanding of evolution.

As the extended title of her book points out, Zuk feels that the paleofantasy extends well beyond the current diet fad. It influences beliefs about health and illness, about family life, about sex. (This last is the focus of all sorts of wistful imaginings: the book provides an entertaining sample of these.) Do bonobos, for example, really provide a good model for how human sexual activity might have been before modern mores took over? I can’t see it myself: humans and their chimpanzee cousins have follwowed separate evolutionary trajectories for 5-6 million years, and there’s no good reason why either species should closely resemble the last common ancestor. And that goes for aspects of intimate morphology as much as for behaviour: I did not know that chimpanzees have penis spines –  ”hardened growths that may serve to sweep away the sperm of previous mates.”

Zuk concludes that the paleofantasy is just that, a fairy tale – and one that limits our understanding of our own biology and evolutionary history:

But to assume that we evolved until we reached a particular point and now are unlikely to change for the rest of history, or to view ourselves as relics hampered by a self-inflicted mismatch between our environment and our genes, is to miss out on some of the most exciting new developments in evolutionary biology.

 

Anyone interested in hearing Professor Zuk speak should check out the details of her upcoming lecture tour. I’ll be grabbing a ticket to the Hamilton event!

 

gmo myths & mythinformation Alison Campbell Jul 28

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The GMOLOL group on Facebook regularly posts on the subject of Genetically Modified Organisms (GMOs) and more recently – like many other pages – about the outrageous claims by the self-styled “Health Ranger” about Monsanto, likening the company & pretty much anyone with anything positive to say about GMOs to the Nazi regime of WWII. (NB he’s actually gone back & added a ‘preface’ to the original post at that link, due at least in part to the internet fuss that followed his original posting.) Fairly soon after another webpage posted names & details of scientists working on or speaking in favour of GMOs, which was unsurprisingly viewed as quite threatening by at least some of those named. There’s an interesting bit of forensic work on the 2 pages & the sequence in which they appeared here. And Orac has a thoughtful commentary here.

It was also not a surprise to see the Ranger using myth to make his case: claiming here, for example, that GMOs have led to widespread farmer suicides in India. No sense in letting the truth get in the way of a good story, I suppose. Especially when it turns out to be rather more complex.

Of course, he is ignoring the fact that we have been selecting for genetically modified organisms for at least as long as we’ve had agriculture and domesticated animals. Sweetcorn or watermelons, anyone? Let alone that horizontal gene transfer is an excellent mover of genes that can link widely separated taxonomic groups; this example of fungi using bacterial genes to form nodules on plant roots is a case in point.

I’m guessing he wouldn’t like the idea of GM insulin or using GM mosquitoes to control the spread of dengue fever, either.

The internet can be a fun place to play & to find information, but alas! it’s also made it so much easier to spread mythinformation to a much wider audience than ever before.

secrets from an ancient graveyard Alison Campbell Dec 16

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One of my current favourite TV programs is Time Team – I enjoy learning little bits of history & Tony Robinson’s happy enthusiasm is so contagious (but I still think of him as Baldrick). So you’ll understand that I was happily distracted this morning when, while looking for something else (isn’t that usually the way?), I stumbled across a fascinating piece about an ancient graveyard in the Italian town of Badia Pozzeveri.

Published on Science magazine’s site, the article tells the story of the ongoing excavation of a medieval graveyard. The dig is providing a wealth of information on things like the dietary differences between nobles, monks, & peasantry (based on isotope analysis of their teeth) & the impact this had on health. What’s more, using ancient DNA (aDNA) techniques, the scientists leading the dig are hoping to identify the presence of various pathogens, such as Yersinia pestis (the bacterium linked to the Black Death, and which still causes cases of plague in the US today) and Treponema pallidum, which causes syphillis and has already been found in 16th-century mummies from Naples.

And like many episodes of Time Team, the tale has a twist at the end: a bit of fashion-based detective work showed that at least some of the burials were not medieval at all.

selecting for maladaptive behaviour Alison Campbell Dec 13

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One of the questions that often comes up in my first-year bio classes relates to natural selection and human evolution. Does the fact that modern medical science keeps alive people who in previous centuries might have died, mean that we’re countering the effects of natural selection? As you can imagine, this generates quite a lot of interesting discussion that spans ethical issues as well as the obvious biological ones.

Next year I think I’ll give the class a new paper to read: one that examines such a question in the context of the Chatham Island black robins (Petroica traversi) (Massaro et al, 2013).

As many New Zealand biology students may know, by 1980 the breeding population of this little bird was reduced to a single pair, in a total population of seven. Things were not looking good, but dedicated conservation workers – led by the late Don Merton (there’s a lovely obituary for him here) – managed to turn things around by careful management of the population, including fostering the robin’s first clutches under another species (thus inducing the robins to lay again), and translocating the small population from Little Mangere Island to the better habitat on Mangere Island. However, it seems that at the same time, the conservationists were also unwittingly selecting for a distinctly maladaptive behaviour – that of laying eggs that were left teetering on the very brim of the nest.

After that initial bottleneck event the population slowly started to recover. However, the researchers working with them noticed that in 1984 one of the five breeding females laid a sinlge egg were laid at the edge of her nest, with more females following suit in subsequent years. Left alone the eggs didn’t hatch, mainly because they weren’t incubated (although I suspect some could simply fall off the edge). The obvious thing to do was to reposition the eggs in the nest, & this resulted in an increased in chicks hatched & subsequently fledged. However, Massaro & her colleagues report that by 1989 18 of the 35 females (51%) were ‘edge-layers’, a behaviour that would leave the population completely reliant on human intervention if edge-laying continued to spread.

The research team suspected that this was an example of inherited rather than learned behaviour, and hypothesised that

[if] rim-laying [had] a genetic basis, and its spread [had] been facilitated by human intervention through egg repositioning, the frequency of this trait would be predicted to decrease following cessation of intervention.
Conservation workers stopped moving rim eggs in 1990, which then meant that the researchers could subsequently compare data sets:
we therefore compared egg-laying data from three years before cessation of repositioning (1987–89) with a three year period almost two decades after management stopped (2007–09)

and found that the number of rim eggs being laid decreased significantly between those two periods. They next looked at the many years’ worth of data to see if the ‘rim-laying’ behaviour had any effect on individuals’ evolutionary fitness, and discovered that

[when] rim eggs were not repositioned, females that laid rim eggs had significantly reduced clutch sizes (i.e. number of eggs laid inside nests that were incubated), and decreased hatching and breeding success compared to normal-laying females, demonstrating that rim laying substantially reduces fitness.
The final step was to confirm that this maladaptive behaviour did have a genetic underpinning. This part of the study was aided by the fact that there’s an extensive genetic pedigree available for this closely-studied species. Examining that pedigree, Massaro & her co-workers found that a) the behaviour first showed up in the grand-daughters of the ‘founding’ female, ‘Old Blue’; and b) that the population was highly inbred. A detailed analysis of the pedigree led them to determine that the rim-laying trait was an autosomal dominant trait that’s inherited in a Mendelian manner (ie no evidence of sex-linkage). Their final message:
This episode yields an important lesson for conservation biology: fixation of maladaptive traits could render small threatened populations completely dependent on humans for reproduction, irreversibly compromising the long term viability of populations humanity seeks to conserve.

 

You’ll also find information on the study here on the University of Canterbury website.

Massaro M., Sainudiin, R., Merton, D., Briskie JV, Poole, AM, Hale ML (2013) Human-Assisted Spread of a Maladaptive Behavior in a Critically Endangered Bird. PLoS ONE 8(12): e79066. doi: 10.1371/journal.pone.0079066

 

migration and ear wax Alison Campbell Nov 08

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Last year’s Schol Bio paper contained (as is usual) some interesting and challenging questions. One of them was about earwax. More specifically, the earwax phenotypes ‘dry’ and ‘wet’, and what their distribution can tell us about patterns of human evolution. (Note to those sitting these examinations: most questions have a reasonable amount of resource material provided and this one was no exception. Remember to use this information in your answers! Ignoring it, or – just as bad – copying bits rather than incorporating the material properly – is not a sign of a good response.)

I was particularly interested in this question because we used to look at the distribution of various phenotypes, wet & dry earwax among them. The examiner provided information about the nature of the genetic information underpinning the two phenotypes, along with data about the global distribution of people with wet & dry wax in their ear canals, including a very helpful map. The following graphic is not that map, but is very similar – showing allele frequencies rather than the phenotype distributions used in the exam – & accompanies an excellent blog post on the Discover magazine site. The ‘A’ and ‘G’ represent the 2 alleles involved in determining the relative dampness of your earwax:

Earwax is wet unless an individual has Adenine (A) at a particular site instead of Guanine (G), in which case the wax becomes the dry form. People who inherit the version of the gene that has A from both parents have dry earwax. People who inherit two of the G versions, or one G and one A, have wet earwax.

The actual question asked candidates to

use biological knowledge, together with information from the resource material, to discuss:

  • the origins and inheritance patterns of dry earwax
  • the evolutionary factors that may have resulted in the present-day distribution of both types of earwax.

And as always, a successful candidate would address all parts of a question. Nor would they assume that the examiner ‘knows’ what they know – you do need to spell out your understanding.

So, for the first bullet point: we’re dealing with a substitution mutation, where a change in a single base (from G to A) has led to a single amino acid change in the final protein. That secretory protein’s function is altered so that the wax that’s produced is now ‘dry’. The mutation must have occurred in a gamete-producing cell, or at the least during meiosis, & subsequently entered the human population’s gene pool. We know it’s a recessive mutation as someone must be homozygous for the allele to express wet wax, while heterozygotes have dry earwax. And you could also add that it’s not a sex-linked mutation, because (as the resource material notes) the gene involved in wax secretion is found on chromosome 16.

The second part of the question requires you to relate the information on the distribution of ‘dry’ & ‘wet’ wax phenotypes to your knowledge of patterns of human dispersal (in this case, the ‘out-of-Africa’ model). The fact that there’s no ‘A’ allele in African populations suggests that this mutation must have arisen after our species started to spread out of Africa. Furthermore, it could well have appeared once a small founder population had arrived in China, with subsequent genetic drift removing the dominant (G) allele from that founder group – this would explain the very high frequency of the A allele (up to 100%) in that region. You could also argue the possibility of positive selection pressure on this version of the secretory protein (an idea critiqued by the author of the Discover blog post).

However, the A allele is also found at fairly high frequencies in other Asian countries – the most likely explanation here is that subsequent migration and interbreeding has introduced it to those populations (with 54% of Indians and 69% of Japanese now expressing the ‘dry’ phenotype). Until fairly recently there was only minimal migration from China into Russia & Europe, which accounts for the very low frequency of the recessive allele in those populations.

What about the Americas? Our current understanding is that humans migrated into North America from Asia via a land bridge across the Bering Strait, during a glacial period. (There’s an interesting discussion around this here, including some work done using a molecular clock based on mutations in the common human pathogen Helicobacter pylori to estimate migration paths & times.) In dealing with this part of the question, I can think of a couple of options: that the lower frequency of the A allele in native American peoples reflects a founder event where the allele was at lower frequency to begin with, & subsequent genetic drift; or that the A allele frequency originally reflected that in Asian populations, but was diluted by a significant drop in population size following European settlement & some later interbreeding with the settlers. Simiilarly, the low A frequency in non-native Americans simply reflects their relatively recent arrival from Europe.

Who’d have thought that the story of earwax could be so fascinating?

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