Posts Tagged genetics

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


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


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 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.




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!


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


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.

a little extrapolation is a dangerous thing Alison Campbell Apr 19


The other day one of my friends sent me a link to this discussion of a recently published paper. (‘Published’ in the sense that it’s available through archiv arXiv, which I gather means it hasn’t been through peer review.) The actual paper is available here. Basically, the authors claim that life has increased in complexity – they’ve used genome size as their measure – as it’s evolved, and that extrapolating that trend backwards suggests that life evolved prior to the formation of the solar system.

But is genome size a particularly good proxy for complexity? Here’s the graph that underpins the conclusions reached by Sharov & Gordon:complexity vs time.jpg

Do you see what they’ve done there? ‘Worms’ – which worms? For after all, there are a lot of them: at least 10,000 species of flatworms, more than 80,000 species of roundworms (aka nematodes), and another 10,000 or so annelids (including the familiar earthworm), not to mention the less familiar taxa such as velvet worms & the priapulids. As for the arthropods – well, good old Daphnia has more functional genes than we do. (The poetical Cuttlefish has a nice take on this story here.)

And I see that plants & protists have been left out altogether – unless they’ve been lumped in under the general heading ‘eukaryotes’. Which is strange, because the overall genome size varies by 5 orders of magnitude** across the eukaryotes so far studied, so using a whole bunch of data points instead of the collective average, would make more sense. Unless that would spoil the nice straight line? (**Having said that, much of that variation is due to the number of introns & the quantity of non-coding DNA; however, the various regulatory sequence regions must surely come under the authors’ heading of ‘functional non-redundant genome’?)

I had also thought, on reading the review, that we were probably looking at an argument for panspermia. And I was right. This and other conclusions are presented in the abstract, & I note a certain amount of hubris in the assumption that humanity represents the only possibility of intelligent life in our universe (my emphasis).

(1) life took a long time (ca. 5 billion years) to reach the complexity of bacteria; (2) the environments in which life originated and evolved to the prokaryote stage may have been quite different from those envisaged on Earth; (3) there was no intelligent life in our universe prior to the origin of Earth, thus Earth could not have been deliberately seeded with life by intelligent aliens; (4) Earth was seeded by panspermia; (5) experimental replication of the origin of life from scratch may have to emulate many cumulative rare events; and (6) the Drake equation for guesstimating the number of civilizations in the universe is likely wrong, as intelligent life has just begun appearing in our universe.

A.A.Sharov & R.Gordon (2013) Life Before Earth arXiv:1304.3381v1  

PS Strangely, in a paper supposedly about biological evolution, the latter part of the article goes on to discuss technological (ie cultural) evolutionary change – I’m not convinced that it’s appropriate to segue between a claimed link for genetic complexity & time, into the undoubted complexity and rapid ‘evolution’ of technology; apples & oranges, guys.

cloning neandertals – can we? should we? is it true? Alison Campbell Jan 23


The Telegraph has a story on the possibility of cloning Neanderthals, with the fetching headline: ‘I can create Neanderthal baby, I just need willing woman.’ (You can read the NZ version on Stuff.)

My first thought was ‘eeewww’. (And, as a friend commented, it’s stories like this that get science a bad name.) Once past that rather visceral reaction, various questions popped up: just how feasible is this? Really? Has the researcher given any consideration to the ethical issues such a proposal generates? What about (epi)genetics, ecology & so on? And – for the money – how much of this ‘story’ accurately reflects what the scientist who was interviewed actually said, & how much of it is.. er… down to a combination of poor translation (the original article was in German-language paper Der Spiegel) and journalistic license?

Let’s deal with the last first: it would appear that the Daily Mail is responsible for the form in which this story hit the English-speaking world (oh, why am I not surprised by this?). And indeed, one of the quotes attributed to Harvard geneticist Professor Church strongly suggests the journalist wasn’t paying attention:

The professor claims that he could introduce parts of the Neanderthal genome to human stem cells and clone them to create a foetus that could then be implanted in a woman.

‘Parts’ of the genome would give you a Neanderthal? Implanting a ‘foetus’? Hellooooo.

Prof. Church is very firm that he hasn’t actively sought out volunteers for any potential, very-much-in-the-future surrogacy program. Rather, he was speaking theoretically of what was possible now that the Neanderthal DNA sequence is known. That’s good to hear, but I can’t help thinking that a little forethought might have avoided this whole furore. Science & scientists don’t need this sort of press. And let’s face it, people are more likely to remember the shock! horror! of the original story than they are to recall the subsequent, much less ‘exciting’ correction.

On the ethics front, bringing back an extinct race of humans from the dead (apart from the fact that there’s a little bit of their DNA in most of us) strikes me rather as treating them as objects. And what would be the justification for that? While there’s plenty of evidence that there are individuals around today who view other people in much the same way (ie as objects with no real rights or feelings about what’s happening to them), that is hardly a moral justification for resurrecting the Neanderthals. (And, before someone ever got to the point of cloning, there’d have to be some very serious examination of the ethics of surrogacy in a situation such as this.)

And what of the fact that they’d be brought back to an environment quite different to the one to which natural selection had shaped them? For example, in addition to having a physique (& probably physiology) best suited to cold environments, any cloned Neanderthal would be lactose-intolerant. And, in life, Neanderthals would have had their own microbiome: their own suite of micro-organisms living on and in their bodies and affecting them on a daily basis. For this hypothetical cloned individual, what would be the effect on their health of a microbiome that didn’t ‘match’?

On the genetics front (& Grant or David might like to comment here), there is a big difference between knowing the complete Neanderthal base sequence (or at least, the base sequence derived from a handful of individuals) and having a nuclear genome in a form that can be inserted into an enucleate egg (or stem cell, which was the focus of part of Prof. Church’s discussion with Der Spiegel). Plus, that wouldn’t be enough – the mitochondrial DNA of the egg cell would need to be replaced with Neanderthal mtDNA. Not to mention the effect of epigenetics on expression of those Neanderthal genes.

Yes, definitely some good learning opportunities there. I must try & work some of them into my own classes.

stem cells, cosmetics – and unexpected consequences Alison Campbell Jan 12

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I’m starting to think about this year’s teaching: what I’m planning, what worked last year & what didn’t, things that need to be revised. One thing I’ll be doing a bit more of is ‘flip teaching’, something that worked well last semester in helping students learn about & gain an understanding of recombinant DNA technologies. I’d already found that for this particular topic, students seemed to gain far more from tutorial-group discussions rather than the lecture itself, and so tried something  a bit different. The class could view a previous lecture recording, plus look at my updated powerpoint slides, before class, and then in the actual lecture I spent about 5 minutes setting the scene, gave them some ‘starters’ for discussion (based on things that had come up in those tuts), and 10 minutes for small-group discussion (which was happy, noisy, & extremely animated) while I circulated & answered questions. Then we came up with a list of ideas & topics generated by those groups, & the discussion began. It was interesting & stimulating & fun – well, that was my impression & the class  feedback suggested that the students found it extremely valuable. Which is great as that was my hope & intention in setting things up that way.

Anyway, one of the topics was stem cells (something I blogged about quite a while ago now), & we talked quite a bit around things like ethics, as well as the practicalities. And the potential risks. Reviewing this particular class, I was reminded of a recent Scientific American article about an unexpected and undesirable outcome of a cosmetic use of stem cells.

Now, stem cells are in the news periodically, often in relation to desperately-ill people who are willing to try just about anything in the hope of achieving a cure. And certainly there is ongoing research into the use of stem cells for things like motor neurone disease, for example. However, the US Food & Drug Administration has so far approved just one stem cell product: the use of cells derived from umbilical cord blood as a treatment for leukaemia.

But cosmetics? Well, yes. Apparently there are quite a few cosmetic uses of stem cells out there – in fact, I’d previously come across the promotion of extract of apple stem cells as a skin rejuvenation treatment. (They are said to come from a strain of apples where the fruit keeps very well & doesn’t wither… And I must say, it was a pleasant surprise to see the Daily Mail being reasonably sceptical of this one.) But these uses can have rather unexpected consequences.

In this particular case, back in 2009 a woman had undergone a ‘facelift’ that used her own adult stem cells taken from abdominal fat: specifically, mesenchymal stem cells, which can differentiate into the cells that make up fat, bone, & cartilage. These cells had been cultured & then injected into the woman’s face, particularly the area around her eyes, where they would supposedly stimulate growth of new cells and help repair existing tissues. The process went well, but 3 months later she consulted another cosmetic surgeon, telling him that it hurt to open one eye – & that when she did, she heard a strange clicking noise. The surgeon ended up removing pieces of bone from her eyelid and the tissue around her eye – these were the source of the clicking noise, & they’d also scratched the surface of her eye.

Why bone? Because during the original treatment the doctor had injected a dermal filler, routinely used to reduce wrinkles by ‘filling’ them in. (The cynic in me wonders whether any perceived improvements in appearance were due to this, rather than the action of stem cells.) These fillers contain a substance called calcium hydroxylapatite – used by cell biologists to trigger differentiation of mesenchymal stem cells into bone; in other words, this outcome could have been predicted.

So, unregulated treatments may well pose risks for consumers. In addition, they may also indirectly affect research into possible applications of stem cells in therapies for actual, serious illness (in contrast to what one could describe as ‘vanity’ treatments), as the Scientific American article concludes:

Beyond the considerable risks to consumers, unapproved stem cell treatments also threaten the progress of basic research and clinical trials needed to establish safe stem cell therapies for serious illnesses. By harvesting stem cells, subsequently nourishing them in the lab and transplanting them back inside the human body, scientists hope to improve treatment for a variety of medical conditions, including heart failure, neurodegenerative disorders like Parkinson’s, and spinal cord injuries—essentially any condition in which the body needs new cells and tissues. Researchers are investigating many stem cell therapies in ongoing, carefully controlled clinical trials. Some of the principal questions entail which of the many kinds of stem cells to use; how to safely deliver stem cells to patients without stimulating tumors or the growth of unwanted tissues; and how to prevent the immune system from attacking stem cells provided by a donor. Securing funding for such research becomes all the more difficult if shortcuts taken by private clinics and cosmetic manufacturers – and the subsequent botched procedures and unanticipated consequences – imprint a stigma on stem cells.

I’ll be giving this article to my 2013 class to read. It should provoke some interesting discussion.


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