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Posts Tagged genetics

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.

a little extrapolation is a dangerous thing Alison Campbell Apr 19

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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

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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.

 

how do kids learn about dna? Alison Campbell Sep 30

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My significant other is forever telling me that Facebook is a total time-waster. Sometimes I do tend to agree – but also, one can Find Out Stuff! Like the study I’ve just heard about via Science Alert, on how children get information about genetics and DNA – things we might regard as being in the ‘too hard’ basket & so best left for senior high school students to grapple with. That grappling begins in year 11, when one of the NCEA Level 1 Science standards asks that students be able to “demonstrate understanding of biological ideas relating to genetic variation”.

Is that too late? Jenny Donovan and Grady Venville suggest that it is, arguing that with the rapid growth of knowledge in and applications of molecular biology,

[citizens] of the future will be called upon to make more decisions, from personal to political, regarding the impact of genetics on society. ‘Designer babies’; gene therapy; genetic modification; cloning, and the potential access to and use of personal genetic information are all complex and multifactorial issues. All raise ethical and scientific dilemmas.

They give the example of jury trials, where jurors may hear quite complex information about DNA and be asked to consider this in coming to a verdict, and note that people may have acquired a range of misconceptions around DNA from sources such as the popular program CSI and its various spin-offs.

Children, for example, have a lot of opportunity to hear about genes, DNA, & their uses well before we start formally teaching these concepts at school. Donovan and Venville already knew (from their own previous research) that by the end of their primary schooling many students were already developing misconceptions about genetics; for example, the idea that ‘genes and DNA are two totally separate entities.’ This time, they wanted to examine the impact of the mass media on children’s conceptions (& misconceptions) around this subject. The misconceptions part is particularly important because misconceptions, once formed, can be extremely persistent – affecting learning into the tertiary years.

Using a combination of interviews and questionnaires about media use, the researchers found that their subjects (children aged 10-12) spent around 5 hours a day using various media (TV, radio, print media, movies, & the internet), with most of that being watching television. This included crime shows, and the children felt that they gained most of their ‘knowledge’ of genetics from TV. Donovan & Venville chose to question children from this age group because, with falling numbers of Australian students taking science subjects in upper secondary school, ‘exposure to genetics may be their sole opportunity to develop scientific literacy in this field’ – where ‘scientific literacy’ encompasses literacy both within and about science.

So, what did they find out?

Most children (89%) knew [about] DNA, 60% knew [about] genes, and more was known about uses of DNA outside the body such as crime solving or resolving family relationships than about its biological nature or function. Half believed DNA is only in blood and body parts used for forensics.

Very few – only 6% – knew that DNA and genes were structurally related. Around 50% of the children surveyed felt that DNA & genes are found in only some tissues & organs. (I was half expecting them to say that DNA is found only in genetically-modified organisms – with GMOs in and out of the news, it’s odd that this didn’t come up.) And 80% of them felt that TV was ‘the most frequent source of information about genetics (with teachers confirming that the subject hadn’t been taught at school). As a result of these findings, Donovan & Venville argue very strongly that instruction in genetics should take place much earlier in students’ time in school, noting that other researchers suggest that

giving students opportunities to revisit science ideas and build deeper understanding over time, enables them to grasp and apply concepts that typically are not fully understood until several years later… [and that] students need to be exposed to background knowledge from early ages in order for them to make sense of what they absorb from the world around them.

So, if kids are going to watch programs like NCIS, CSI, and Bones on a regular basis, then maybe early teaching around genetics concepts could use

lively discussions around what they have seen and heard about genetics in the mass media [as this] may ultimately help children to make informed decisions in their future lives.

An interesting suggestion – and one which reinforces yet again how important proper resourcing and support of science teaching are, if we are to develop real literacy in and about science.

J.Donovan & G.Venville (2012) Blood and bones: the influence of the mass media on Australian primary school children’s understandings of genes and DNA. Science & Education (published online 23 June 2012, doi: 10.1007/s11191-012-9491-3

more on mosaics Alison Campbell Sep 06

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A couple of days ago I posted a stunning photo of a peacock, and talked a bit about the possible genetic underpinnings of its colour patterns. My friend & blog-buddy Grant then pointed me at the story of a cat that has a similarly amazing colouration. Venus even has her own Facebook page! (I will definitely be using both these images & their stories with my first-year class next week.)

As you can see,  one half of Venus’s face is black, with a yellow eye, while the other half is orange – with a blue eye. What a stunning cat!

The underlying reason for her striking colouration isn’t clear. She could be a chimera, formed from the fusion of two fertilised eggs, so that some of her cell lines would have different DNA from the rest. She could equally well be a particularly impressive example of the results of X-chromosome inactivation in female mammals. In that case, of the two X chromosomes in the cells of the right-hand-side of Venus’s face, the one with the ‘orange’ allele would have been inactivated. That side of her face is black because all cells have functioning X chromosomes that are expressing the ‘black’ allele. The reverse would be true for the orange side of her face.

Which leaves the question: why does she have a blue eye on the orange side?

In the comments thread to my original post, herr doktor bimler noted that

[the] X-chromosome mosaicism of female mammals turned up a lot in colour-vision research, because women carrying a colour-deficiency gene on one X chromosome end up with their retinas being more-or-less coarse patchworks of colour blindness. In the extreme case people can be red-green deficient in one eye and normal in the other**.

This can also be true for haemophilia, where the gene locus involved in the most common form of this disease is found on the X chromosome. (Haemophilia C is not sex-linked.) Heterozygous women, with one normal and one recessive, deleterious allele, are regarded as carriers, unaffected but with the potential to pass the ‘haemophilia’ allele on to some of their children, with damaging effect in those sons who receive it. But – and I must get my class to consider this one next week – such women are mosaics for X chromosome genes. If the ‘haemophilia’ X chromosome is ‘on’ in all the cells of their bone marrow, those women would also be haemophiliac.

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**Being a person with a dry sense of humour, herr doktor concluded that such women “must spend their lives hiding from the colour vision researchers who wish to experiment upon them.”

immortal cells Alison Campbell Sep 05

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Last year one of the books on my reading list was The Immortal Life of Henrietta Lacks, by Rebecca Skloot. I found it a fascinating and moving story. Henrietta Lacks died of cervical cancer, but even before her death doctors had begun to culture cells removed from her cervix (something that was done without her knowledge). Amazingly, these cells didn’t divide a few times and then become senescent; instead, they continued – and continue – to divide without end. HeLa cells are probably one of the most widely used cell lines (they’ve even been up in space) and in that sense, something of Henrietta lives on today.

Recent research indicates that the same is true of the clonal cell line implicated in the Devil Facial Tumour Disease that is killing Tasmanian devils (with population declines of up to 90% in some parts of Tasmania), spread via bites inflicted during social interactions. From the paper just published in PLoS One (Ujvari et al, 2012):

Devil Facial Tumour Disease (DFTD) is a unique clonal cancer that threatens the world’s largest carnivorous marsupial, the Tasmanian devil (Sarcophilus harrisii) with extinction. This transmissible cancer is passed between individual devils by cell implantation during social interactions. The tumour arose in a Schwann cell of a single devil over 15 years ago and since then has expanded clonally, without showing signs of replicative senescence; in stark contrast to a somatic cell that displays a finite capacity for replication, known as the “Hayflick limit”.

DFT cells are apparently stable chromosomally, and the tumour cells of different individuals are genetically identical – rather surprising since the tumours have proliferated and their cells passed on to thousands of Tasmanian devils in the short time since DFTD was first identified. This capacity for seemingly endless division is due to the action of the enzyme ‘telomerase’ on structures called telomeres, found on the ends of eukaryote chromosomes.

Normal somatic (body) cells replicate only a few times and then enter ‘replicative senescence’ (Uvjari et al. 2012). This is because the telomeres – tandem DNA repeats bound up with a particular protein complex called ‘shelterin’ – shorten each time the cells divide. The only ‘normal’ cells where this doesn’t happen ** are the cells that give rise to eggs and sperm, due to the action of telomerase, which maintains the length of the telomeres. The same is true for cancer cells.

DFT cells have quite short telomeres, and the research team found that their length is maintained through up-regulation of telomerase gene expression; the shelterin protein complex protects them from continuous elongation. What’s more, it seems that this control is done at the level of individual cells, with up-regulation in cells where telomeres have become shorter over several cycles of cell division, and shelterin blocking further elongation of ‘normal-length’ telomeres. Ujvari & colleagues suggest that

The short telomeres and up-regulation of telomerase likely counteract each other. The short telomeres lead to increased genetic instability but the telomerase activation facilitates tumour growth by either inhibiting further chromosomal instabilities or by circumventing checkpoints that recognise dysfunctional telomeres. Longer telomere lengths may ensure the success and survival of DFT cells by stabilising chromosomal rearrangements and preventing further genomic instabilities.

These features of DFT cells promote survival of the tumours and are the result of natural selection. Coming to a better understanding of the evolution of these features in DFTD could offer useful insights for those seeking to understand tumour development in our own species.

Ujvari B, Pearse A-M, Taylor R, Pyecroft S, Flanagan C, et al. (2012) Telomere Dynamics and Homeostasis in a Transmissible Cancer. PLoS ONE 7(8): e44085. doi:10.1371/journal.pone.0044085

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In other intriguing research, it appears that mice engineered to have no functioning telomerase age more quickly than normal, but that this decline may be reversed by switching the enzyme back on through adding a particular chemical to their diet. I suppose I should not be surprised to see that the woo-meisters have seized on this: you can purchase a dietary supplement that claims to achieve the same effect in humans (if the glowing testimonials can be believed…)

 

a genetic chimera? Alison Campbell Sep 04

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I used to enjoy watching CSI (the original series), back when Gil Grissom (actor William Petersen) headed that fictional forensics lab. It was never the same after he left.

Anyway, one episode that I still remember involved a crime being committed by someone who was a genetic chimera: someone who had developed from an embryo formed when two fertilised eggs fused together. (There’s a fascinating blog post about chimeras over at damninteresting.com.)The upshot was that some cell lines in that indivdual’s body had one set of DNA, with other cells having a different genetic makeup. In such individuals it’s possible for different tissues to express genes from one or the other lot of DNA, something that’s called mosaicism (it’s also possible in all female mammals, where one or the other X chromosome is randomly inactivated when the embryo is at around the 1000-cell stage of development).

I was reminded of that episode when I saw this photo on Science Alert’s Facebook page (ah, the wonders of modern social networking!):

You’d need to look at the DNA from the white & ‘normal’ sides of this bird to be sure whether what we’re seeing here is definitely the result of a chimera displaying mosaicism. But isn’t it a stunning image?

science – it’s not magic! Alison Campbell Aug 31

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One of the things I like about my job is that there’s always the opportunity to learn new things. Today I learned about episomes. Not being an actual geneticist & all, it was a novel term to me. An episome is defined as:

a portion of genetic material that can exist independent of the main body of genetic material (called the chromosome) at some times, while at other times is able to integrate into the chromosome.

By that definition, transposons and viruses would both be episomes, while bacterial plasmids aren’t, because they don’t insert themselves into the main bacterial chromosome.

I learned about them as a result of discovering that Bad Science Reporting is always out there somewhere, courtesy of my blogging buddy Aimee, who sent me this link to a report on how scientists have cleared a path to the fountain of youth. Yes, really.

It’s an article about some rather interesting research into the possibility of reprogramming adult cells so that they return to a pluripotent stem cell state. (You can read the original paper here at PLoS One: the genetics is a bit technical but the intro & discussion are reasonably straightforward.) Reprogramming somatic cells often uses viruses, which can be problematic if the viral DNA inserts into the ‘wrong’ place in the recipient cells’ genomes, but if transfection agents aren’t used then conversion of body cells to stem cells tends to have a very low success rate: the authors of the PLoS One paper give a figure of 0.001% to 0.5% (Park, Huo, Peters, Talbot, Verma, Zimmerlin, Kaplan & Zambidis, 2012).

However, the researchers report figures of around 50%, which is quite something. They did it using cord blood (ie umbilical cord blood), where the cells were ‘lineage committed’ ie they had already differentiated from the pluripotent state, and tweaking gene expression in those cells using ‘episomal nucleofection’ to carry a set of four key genes into the cells’ nuclei. (The earlier you catch cells post-differentiation, the easier it apparently is to nudge them back to pluripotency: ‘developmentally immature’ cells (Park et al., 2012) will revert at a higher rate than fully differentiated adult cells.)

So, preliminary proof of concept, but a long way from inducing adult tissue cells to re-enter a stem cell state.

Unfortunately, the writer of the article Aimee pointed me at seems to have been a little overenthusiastic in their reporting:

an efficient and totally safe method to turn adult blood cells [back to their embryonic state]. The discovery could be the key to cure the incurable – from heart attacks to severed spinal cord to cancer – and open the door, some day, to eternal youth.

For some reason the article talks of obtaining ‘adult blood cells’ from a patient’s spinal cord, when the original paper talks of cord blood from a cord blood bank (ie we are talking umbilical cords). It also mentions plasmids, when the paper talks of episomes. (I guess that one’s less obvious as I thought ‘plasmids’ on first reading & had to look up episomes for myself!).

As for ‘totally safe’ – hmmm, that one I would want to hear more about. Plasmids don’t integrate into host DNA, but episomes do – so the potential is still there for disruption of functional genes. But the phrase that nearly made me cough tea over the keyboard was this:

the cultivated cells magically turned to embryonic stem cells.

No, no, no! The researchers are able to describe the mechanism. They are pretty clear on what has happened. This is SCIENCE, not some magical intervention!

I will leave my readers to debate whether this final vision of a brave new world is necessarily one to look forward to:

Hypothetically, if you’re able to perpetually fix any part of your body, there’s no reason you wouldn’t be able to live as long as you wanted.

 

Park TS, Huo JS, Peters A, Talbot CC Jr, Verma K, et al. (2012) Growth Factor-Activated Stem Cell Circuits and Stromal Signals Cooperatively Accelerate Non-Integrated iPSC Reprogramming of Human Myeloid Progenitors. PLoS ONE 7(8): e42838. doi:10.1371/journal.pone.0042838

reflections on the WEB days Alison Campbell Jun 13

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We’ve just held the second day of the annual “Waikato Experience of Biology” (WEB) days – around 700 year 13 biology students, & their teachers, have come on campus over those 2 days for a program of seminars + some lab experience that supports their learning in several areas of their Biology curriculum. (There are photos on the Faculty’s Facebook page.) I give seminars on human evolution & other colleagues talk about gene expression, patterns of evolution, biotechnology, and plant responses/animal behaviour.

The students were great – it’s always fun to spend time talking with young people about biology :-) They were also a credit to their schools – when you’ve got a lecture theatre full of 400 year 13 students, & absolutely no issues with noise or chatter during a talk, then that speaks volumes.

I spoke with a lot of the attending teachers as well, just catching up & making sure that we had things pitched at the right level & were meeting their needs & those of their students. (It sounded like we had things pretty much spot-on.) But we also talked about the impending implementation of the new  (‘aligned’) Achievement Standards at Level 3 – this is the last year that gene expression will be taught & examined at that level, for example, as it’s moving down to year 12 & in its place comes a new AS on homeostasis, and another on ‘human manipulation of genetic transfer’ which seems a more tightly focused version of the previous standard on biotechnology.

And it became quite clear that many of those I spoke with were concerned at how well they were going to be able to deliver this new content & develop their students’ understanding of it. One of the things we’ll be doing here at Waikato to support them is running a teacher evening to provide ideas, content knowledge & maybe other resources. If you’re a scientist with an interest in, say, homeostasis (or cloning, or transgenes), and an interest in communicating the science around it, why not contact the HoD Biology at your local secondary school and offer to help? It could be the start of a wonderful new working relationship :-)

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