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Posts Tagged genetics

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?

essays on our fascination with those who are different Alison Campbell Oct 08

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Book Review: The Two-Headed Boy and Other Medical Marvels 

by Jan Bondeson

Cornell University Press, USA (2004)

Paperback: i-xxii, 297 pages

ISBN: 0-8014-8958-X

RRP: US419.95

It's all Grant's doing, really. If he hadn't picked up on an off-hand comment of mine (relating to vipers in bosoms) & turned that into a catchy blog post, I quite probably wouldn't have gone looking for other books by Jan Bondeson, or found The Two-Headed Boy and Other Medical Marvels

This is a fascinating, saddening, and occasionally appalling book by a humane and extremely well-read author. The subjects of Bondeson's essays are those who are (or were, for these are historical essays) in someway very very different from the rest of us: the exceptionally tall, the enormously obese, the unnaturally hairy, the two-headed boys of the title. Those who in what we'd like to regard as a less-enlightened age would have spent their lives in what were then called 'freak' shows, for others to gawk and gape at. (Not that this horrified fascination with those who are different has disappeared. We just don't deem it appropriate to pay to indulge it.) And while the money may have poured in from the gawkers, all too often most of it made its ways into the pockets of 'managers', and not the afflicted individuals. (Although there were exceptions, which we'll come to shortly.)

One of the things I particularly enjoyed about the book was its interweaving of scientific and historical perspectives. Did Countess Margaret of Henneberg really have 364 – or was it 365 – children all at once? Today we'd immediately say, well of course not! But then, what are the origins of the tale described in Bondeson's essay, "The strangest miracle in the world"? The author examines the development of the legend over the years, noting with wry amusement that until quite recently childless women would wash their hands in the bowl in which the unlikely children were supposedly baptised – even though the original was destroyed long ago. And he shows how science has a part to play in the explanation: it's possible that the Countess delivered a hydatidiform mole. Although you'd think that the midwives might have had some experience of this condition, the mass of small blobby bits might have been seen by them as a large number of gravely undersized babies.

At least Countess Margaret wasn't displayed for money (although the local townsfolk must subsequently have made quite a lot out of tourists), but money's involved in most of the stories. (And attention, which may well have been the driver for the poor lady who pretended to lay eggs – a tale which also attests to the extreme gullibility of those in attendance at the delivery!) Both Daniel Lambert (for a time the fattest-known human, although more recently he has been outweighed by a man nearly double Lambert's 700+ pounds) and the 'Swedish Giant', Daniel Cajanus, parlayed their physical extremes into quite comfortable livings, for not only were they charming and intelligent men but they also had the sense to manage their own affairs. All too often that hasn't been the case, with children put on display out of desperation or greed on the part of parents or 'managers'.

Of those children, I sometimes wonder if our most awful fascincation might not rest on conjoined twins. Bondeson discusses several examples, including parasitic twins and two-headed children. Apparently dicephalus (two-headed) twins represent around 11% of conjoined twins, the great majority of whom die before or soon after birth; certainly a google search will produce more images than you may be comfortable with. I first heard of them when reading Stephen Jay Gould's essay on the twins Ritta-Christina, in which he not only discussed the children's short, sad lives but also the issue of what constitutes an individual. Bondeson also tells their story, but the two-headed boys of his title had a better time of it; in fact, he describes Giovanni and Giacomo Tocci as the "most celebrated pair of dicephalus conjoined twins of all times". While most dicephalus twins are short-lived, often due to other structural abnormalities in one twin or the other, the Tocci brothers were born in 1877 and lived at least into the second decade of the 20th century, at least in part because the boys were 'symmetrical' in that both seemed to have properly-developed hearts and lungs. Like all the dicephalus twins described in the book, the Toccis were two distinct individuals with different personalities and intellects.

And this, of course, poses some serious ethical questions. While it is possible to separate some conjoined twins, depending on the degree to which they share organs and blood vessels, to do this for dicephalus twins means that either both would spend the rest of their lives incapable of independent movement & with significant post-surgical disfigurement, or one would be sacrificed that the other might live. To whom should this decision fall? (The parents of perhaps the most famous living dicephalus twins, Abigail & Brittany Hensel, never considered this option, & their daughters are now young adults.) 

Yes, this is a fascinating and thought-provoking book, not least because it offers a discomforting mirror in which to review how we see those who are so different from ourselves.

 

the origins of humans lie in a – ahem! – far-fetched hybridisation event? Alison Campbell Jul 22

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Or maybe not.

The internet is a wondrous place: a source of information, of amusement, and – alarmingly often – of material that elicits a combination of ‘say what?’ and <head-desk>. And a hat-tip to PZ Myers for this particular example…

For it has been proposed (by the originator of this particular hypothesis, & further discussed on phys.org) that humans arose as the result of an interspecies hybridisation event, rather than the current model for human evolution that sees chimps and humans sharing a Last Common Ancestor 5-6 million years ago and following their own trajectories since that time.

The event? Hybridisation between great ape (specifically, chimpanzee) & wild boar.

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Now, we know that hybridisation happens; that the ‘biological species concept’ is not an absolute. But these events are generally between reasonably-closely related species: hybridisation is quite common in the waterfowl, for example. But even in birds, where hybridisation is well-documented, it doesn’t appear to cross the lines between one taxonomic order and another. Yet the ‘pig+ape’ suggestion requires hybridisation between different taxonomic orders – orders that (so fossil & genetic evidence tell us) have been separate for between 79 & 87 million years.

Surprisingly, Dr McCarthy, a geneticist and the proponent of this novel hypothesis, doesn’t present much in the way of genetic data to support it. He does agree that, genetically, we are closer to chimpanzees than to any other mammal, but suggests that this is due to back-crossing (with the chimp parent) after the initial hybridisation event:

And why might one suppose that humans are backcross hybrids of the sort just described? Well, the most obvious reason is that humans are highly similar to chimpanzees at the genetic level, closer than they are to any other animal. If we were descended from F1 hybrids without any backcrossing we would be about halfway, genetically speaking, between chimpanzees and whatever organism was the other parent. But we’re not. Genetically, we’re close to chimpanzees, and yet we have many physical traits that distinguish us from chimpanzees.

Surely the simpler explanation – that we are genetically similar to chimps because we are sister species – is more likely. Especially since at least some of the differences between the two species can be explained by differences in timing of developmental stages (the relative proportions of face & skull, for example), which may be sheeted home to mutations in regulatory portions of the genome.

In addition, there are major differences both in chromosome number (38 in pigs, 46 in humans) and in the position of various genes on those chromosomes that would make successful gamete production in any hybrid unlikely in the extreme (always supposing the hybrid was actually viable) – PZ discusses this in more length.

But anyway, what about those physical traits that “distinguish us from chimpanzees” & supposedly reflect our shared heritage with pigs? There’s a long list here. Many of them relate to bipedalism; to me, it’s special pleading to suggest that (for example) the presence of large gluteal muscles in bipedal humans and in domestic pigs is evidence of a close evolutionary relationship (Animal Farm aside, there is a distinct lack of evidence for bipedal locomotion in suids – and strong evidence of selective breeding for large backsides in pigs destined to become bacon & pork). Hairlessness? Only in domestic pigs; anyone who’s watched a huntin’&fishin’ show on TV will have seen how hairy a wild boar is. Pigs & humans both have longer hind-limbs than forelimbs, & shorter digits (compared to chimps)? Well, ye-es, I guess so, but that’s hardly evidence for a close relationship; one could say the same of mice… Similarly, while humans & pigs may (usually) be particular about where they defecate, well, so are other animals; rabbits, anyone? As for “snuggling [snuggling???], tears, alcoholism “being shared features in humans & pigs but not chimps… chimps & humans both have an enzyme (alcohol dehydrogenase 4) that allows us to break down ethanol, and it seems that chimps can become addicted to alcohol if given the opportunity.

Also offered in evidence are those diseases which are rare in non-human primates: “heart attack, atherosclerosis, and cancer (melanoma)”. Since these are to some degree, age-related, their relative rarity (for they are not absent in apes) may be ascribed to differences in lifespan: chimps in the wild may not live long enough to develop them.

Annoyingly, I see that over at uncommondescent, this proposal has been presented as even more evidence that evolutionary biologists are Getting It Wrong!

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Perusing more of the macroevolution website, I found the suggestion that armadillos and pangolins evolved from ankylosaurs and stegosaurs (page 244 at that link). It would be interesting to hear a palaeontologist’s taken on that one, but the fact that dinosaurs had diapsid skulls while mammals are synapsid doesn’t help.

 

 

 

 

out of the mouths of students Alison Campbell May 19

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We’ve been trialling some software for on-line paper/teaching appraisals & I got my results back the other day. The appraisal form included open-ended questions where students could give extended feedback on particular issues that concerned them, & I’ve been going through it all so that I can give feedback in my turn, thus ‘closing the loop’. (This is something that I believe is absolutely essential: students need to know that we value their opinions & that, where appropriate, use them to inform what we do.) I’ve been interested to see that some of the class are definitely thinking outside the ‘box’ that represents my paper, and one comment in particular struck a chord:

One concern with the paper is individuals who were not taught certain aspects of the NCEA Level 3 curriculum. This is a major issue that has resulted from the preference of schools to not teach certain aspects of the course. There NEEDS to be consultation to standardise the NCEA curriculum as well as ensuring that the gap is bridged with communication between teriary education providers and secondary education providers. As I understand it there is significant concern over the changed NCEA Level 3 Biology course, which now does not teach genetics in year 13. I don’t know the answer in the resolution of this issue, however it will greaty impact on future acedemic success as well as future funding when grades drop.

This student has hit the nail squarely on the head. Teachers reading this will be working on the following Achievement Standards with their year 12 students this year (where previously gene expression was handled in year 13): AS91157 Demonstrate understanding of genetic variation and change, and AS91159: Demonstrate understanding of gene expression. (You’ll find the Biology subject matrix here.)

And as my student says, this has the potential to cause real problems unless the university staff concerned have made it their business to be aware of these changes and to consider their impact. For the 2014 cohort of students coming in to introductory biology classes will have quite different prior learning experiences (& not just in genetics) from those we are teaching this year and taught in previous years. We cannot continue as we have done in the past.

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