Conservative self-identifies with single-celled brainless organism

Among my usual flood of daily email, I frequently get tossed onto mailing lists for conservative think tanks. Why? I don’t know. I suspect that it’s for the same reason I also get a lot of gay porn in my email: not because I follow it or asked to be added, but because some tired d-bag with no imagination thinks its funny to dun me with more junk. The joke’s on them, though: I might keep it around and skim the stuff now and then to get inspiration for a blog post, and then click-click — a few presses of a button and I add the source to my junk mail filter, and never see it again.

No, I didn’t get inspired by gay porn today, but by drivel from some freakish conservative think tank called the Witherspoon Institute, about which I know next to nothing except that they’re another of those organizations that cloak themselves in the Holy Founding Fathers of America to promote illiberal non-freethinking anti-government BS. This latest is by a philosopher criticizing a book about modern reproductive biotechnologies. He doesn’t like ’em. Not one bit, no sir.

But you know an essay from a philosopher is going to be pretty much worthless when it opens and closes with references to… C.S. Lewis. I don’t know why that man gets so much happy clappy press from believers. I suspect he must have sold his soul to the devil.

Anyway, the bizarre part is in the middle, where Justin Barnard is poleaxed by the author’s, Steven Potter’s, willingness to destroy human embryos. Potter apparently considers several of the sides of the debate, but fails to come down on the side of the Religious Right, that is, that embryos are absolutely and undeniably full human beings from the instant of fertilization, instead espousing the dreadful notion that the definition of personhood falls into a huge gray area.

Potter’s own attempt to wrestle with the morality of destroying human embryos is philosophically, if not biologically, confused from the start. He begins by claiming that “each egg and sperm has the potential to make a person.” Biologically, this is simply false. Gametes, by themselves, have no intrinsic developmental potential for human personhood. Of course, Potter knows this. So his use of “potential” is likely more latitudinarian. Still, three pages later, Potter describes the zygote as having “remarkable potential.” “It can,” he explains, “turn itself into a person.” Ironically, Potter fails to recognize that this potentialist understanding of human personhood is at odds with his rather surprising admission of the embryological facts. Potter writes, “Of course we all began as a zygote. Everyone does.” What is shocking about this concession is what it so obviously entails–an entailment that seems lost on Potter. If I, the human being I am today, “began as a zygote,” then the zygote that began the-human-being-I-am-today was me–i.e., it was a human person. It was not merely a cell with “remarkable potential” to become me. It was me.

If anyone is confused here, it’s Barnard. Of course each egg and sperm has the potential to form a person, especially when we throw biotechnology into the equation, as the book he’s reviewing explicitly does. We already have techniques to revert and differentiate a sperm cell into an egg. For that matter, given time and research, we’ll be able to reprogram just about any cell into a totipotent state, and clone someone from a cheek swab. Does Mr Barnard regard every cell he sheds as a potential person?

Perhaps he wants to argue that a sperm or egg cell doesn’t have the potential for personhood without a human assist. But then by that limitation the zygote has to be excluded as well — no human zygote can develop to term without the extreme cooperation of another individual. Try it; extract a fertilized egg and set it in a beaker by your nightstand, and wait for a baby to crawl out. Won’t happen. A uterus and attendant physiological and behavioral meat construct, i.e., woman, is also an amazing piece of biotechnology that is a necessary component of the developmental process.

But the real blow to this whole “potential” argument is damaged irreparably by Barnard’s last few sentences — was he going for a reductio here? Is the entire essay an exercise in irony? ‘Cause that dope was dumb.

Yes, Mr Barnard began as a zygote. That does not mean the zygote was Mr Barnard. My car began as a stack of metal ingots and barrels of plastics; that does not imply that an ingot of iron is a car. My house began as a set of blueprints and an idea in an architect’s mind; nobody is going to pay the architect rent for living in his cranium or on a stack of paper in a cabinet. The zygote was not Justin Barnard, unless Justin Barnard is still a vegetating single-celled blob, in which case I’d like to know how he typed his essay.

Since Barnard claims to be a philosopher, I’ll cite another, a guy named Aristotle. This is a quote I use in the classroom when I try to explain to them how epigenesis works, in contrast to preformation. Aristotle did some basic poking around in chicken eggs and in semen, and he noticed something rather obvious—there were no bones in there, nor blood, nor anything meatlike or gristly or brainy. So he made the simple suggestion that they weren’t there.

Why not admit straight away that the semen…is such that out of it blood and flesh can be formed, instead of maintaining that semen is both blood and flesh?

Barnard is making the classic preformationist error of assuming that everything had to be there in the beginning: I am made of bones and blood and flesh and brains and guts and consciousness and self-identity, therefore the zygote must have contained bones and blood and flesh and brains and guts and consciousness and self-identity.

It didn’t.

Why not admit straight away that the zygote is such that out of it selfhood may arise, rather than maintaining that the zygote is the self?

In that case we have to recognize that the person is not present instantaneously at one discrete moment, but emerges gradually over months to years of time, that there were moments when self was not present and other moments when self clearly was present, and moments in between where there is ambiguity or partial identity or otherwise blurry gray boundaries. This is a conclusion that makes conservative ideologues wince and shy away — I think it’s too complicated for their brains, which may in some ways be equivalent to the gormless reflexive metabolic state of the zygote — but it is how science understands the process of development.

The new phrenology

Morphological variation is important, it’s interesting…and it’s also common. It’s one of my major scientific interests — I’m actually beginning a new research project this spring with a student and I doing some pilot experiments to evaluate variation in wild populations here in western Minnesota, so I’m even putting my research time where my mouth is in this case. There has been some wonderful prior work in this area: I’ll just mention a paper by Shubin, Wake, and Crawford from 1995 that examined limb skeletal morphology in a population of newts, and found notable variation in the wrist elements — only about 70% had the canonical organization of limb bones.

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I’ve also mentioned the fascinating variation in the morphology of the human aorta. Anatomy textbooks lay out the most common patterns, but anyone who has taught the subject knows that once you start dissecting, you always find surprises, and that’s OK: variation is the raw material of evolution, so it’s what we expect.

The interesting part is trying to figure out what causes these differences in populations. We can sort explanations into three major categories.

  1. Genetic variation. It may be the the reason different morphs are found is that they carry different alleles for traits that influence the developmental processes that build features of the organism. Consider family resemblances, for instance: your nose or chin might be a recognizable family trait that you’ve inherited from one of your parents, and may pass on to your children.

  2. Environmental variation. The specific pattern of expression of some features may be modified by environmental factors. In larval zebrafish, for instance, the final number of somites varies to a small degree, and can be biased by the temperature at which they are raised. They’re also susceptible to heat shock, which can generate segmentation abnormalities.

  3. Developmental noise. Sometimes, maybe often, the specific details of formation of a structure may not be precisely determined — they wobble a bit. The limb variation Shubin and others saw, for example, was almost entirely asymmetric, so it’s not likely to have been either genetic or environmental. They were just a consequence of common micro-accidents that almost certainly had no significant effect on limb function.

When I see variation, the first question that pops into my head is which of the above three categories it falls into. The second question is usually whether the variation does anything — while some may have consequences on physiology or movement or sexual attractiveness, for instance, others may really be entirely neutral, representing equivalent functional alternatives. Those are the interesting questions that begin inquiry; observing variation is just a starting point for asking good questions about causes and effects, if any.

I bring up this subject as a roundabout introduction to why I find myself extremely peeved by a recent bit of nonsense in the press: the claim that liberal and conservative brains have a different organization, with conservatives having larger amygdalas (“associated with anxiety and emotions”) and liberals having a larger anterior cingulate (“associated with courage and looking on the bright side of life”).

Gag.

I don’t deny the existence of anatomical variation in the brain — I expect it (see above). I don’t question the ability of the technique, using MRI, to measure the dimensions of internal structures. I even think these kinds of structural variations warrant more investigation — I think there are great opportunities for future research to use these tools to look for potential effects of these differences.

What offends me are a number of things. One is that the interesting questions are ignored. Is this variation genetic, environmental, or simply a product of slop in the system? Does it actually have behavioral consequences? The authors babble about some correlation with political preferences, but they have no theoretical basis for drawing that conclusion, and they can’t even address the direction of causality (which they assume is there) — does having a larger amygdala make you conservative, or does exercising conservative views enlarge the amygdala?

I really resent the foolish categorization of the functions of these brain regions. Courage is an awfully complex aspect of personality and emotion and cognition to simply assign to one part of the brain; I don’t even know how to define “courage” neurologically. Are we still playing the magical game of phrenology here? This is not how the brain works!

Furthermore, they’re picking on a complex phenomenon and making it binary. Aren’t there more than one way each to be a conservative or a liberal? Aren’t these complicated human beings who vary in an incredibly large number of dimensions, too many to be simply lumped into one of two types on the basis of a simple survey?

This is bad science in a number of other ways. It was done at the request of a British radio channel; they essentially wanted some easily digestible fluff for their audience. The investigator, Geraint Rees, has published quite a few papers in credible journals — is this really the kind of dubious pop-culture crap he wants to be known for? The data is also feeble, based on scans of two politicians, followed by digging through scans and questionnaires filled out by 90 students. This is blatant statistical fishing, dredging a complex data set for correlations after the fact. I really, really, really detest studies like that.

And here’s a remarkable thing: I haven’t seen the actual data yet. I don’t know how much variation there is, or how weak or strong their correlations are. It’s because I can’t. This work was done as a radio stunt, is now being touted in various other media, and the paper hasn’t been published yet. It’ll be out sometime this year, in an unnamed journal.

We were just discussing the so-called “decline effect”, to which my answer was that science is hard, it takes rigor and discipline to overcome errors in analysis and interpretation, and sometimes marginal effects take a great deal of time to be resolved one way or the other…and in particular, sometimes these marginal results get over-inflated into undeserved significance, and it takes years to clear up the record.

This study is a perfect example of the kind of inept methodology and lazy fishing for data instead of information that is the root of the real problem. Science is fine, but sometimes gets obscured by the kind of noise this paper is promoting.

I have to acknowledge that I ran across this tripe via Blue Girl, who dismisses it as “sweeping proclamations about the neurophysiological superiority of the liberal brain”, and Amanda Marcotte, who rejects it because “This kind of thing is inexcusable, both from a fact-based perspective and because the implication is that people who are conservative can’t help themselves.” Exactly right. This kind of story is complete crap from the premise to the data to the interpretations.

The molecular foundation of the phylotypic stage

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When last we left this subject, I had pointed out that the phenomenon of embryonic similarity within a phylum was real, and that the creationists were in a state of dishonest denial, arguing with archaic interpretations while trying to pretend the observations were false. I also explained that constraints on morphology during development were complex, and that it was going to take something like a thorough comparative analysis of large sets of gene expression data in order to drill down into the mechanisms behind the phylotypic stage.

Guess what? The comparative analysis of large sets of gene expression data is happening. And the creationists are wrong, again.

Again, briefly, here’s the phenomenon we’re trying to explain. On the left in the diagram below is the ‘developmental hourglass’: if you compare eggs from various species, and adults from various species, you find a diversity of forms. However, at one period in early development called the phylytypic stage (or pharyngula stage specifically in vertebrates), there is a period of greater similarity. Something is conserved in animals, and it’s not clear what; it’s not a single gene or anything as concrete as a sequence, but is instead a pattern of interactions between developmentally significant genes.

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The diagram on the right is an explanation for the observations on the left. What’s going on in development is an increase in complexity over time, shown by the gray line, but the level of global interactions does not increase so simply. What this means is that in development, modular structures are set up that can develop autonomously using only local information; think of an arm, for instance, that is initiated as a limb bud and then gradually differentiates into the bones and muscle and connective tissue of the limb without further central guidance. The developing arm does not need to consult with the toes or get information from the brain in order to grow properly. However, at some point, the limb bud has to be localized somewhere specific in relation to the toes and brain; it does require some sort of global positioning system to place it in the proper position on the embryo. What we want to know is what is the GPS signal for an embryo: what it looks like is that that set of signals is generated at the phylotypic stage, and that’s why this particular stage is relatively well-conserved.

One important fact about the diagram above: the graph on the right is entirely speculative and is only presented to illustrate the concept. It’s a bit fake, too—the real data would have to involve multiple genes and won’t be reducible to a single axis over time in quite this same way.

Two recent papers in Nature have examined the real molecular information behind the phylotypic stage, and they’ve confirmed the molecular basis of the conservation. Of course, by “recent”, I mean a few weeks ago…and there have already been several excellent reviews of the work. Matthew Cobb has a nice, clean summary of both, if you just want to get straight to the answer. Steve Matheson has a three part series thoroughly explaining the research, so if you want all the details, go there.

In the first paper by Kalinka and others, the authors focused on 6 species of Drosophila that were separated by as much as 40 million years of evolution, and examined quantitative gene expression data for over 3000 genes measured at 2 hour intervals. The end result of all that work is a large pile of numbers for each species and each gene that shows how expression varies over time.

Now the interesting part is that those species were compared, and a measure was made of how much the expression varied: that is, if gene X in Drosophila melanogaster had the same expression profile as the homologous gene X in D. simulans, then divergence was low; if gene X was expressed at different times to different degrees in the two species, then divergence was high. In addition, the degree of conservation of the gene sequences between the species were also estimated.

The prediction was that there ought to be a reduction of divergence during the phylotypic period. That is, the expression of genes in these six species should differ the least in developmental genes that were active during that period. In addition, these same genes should show a greater degree of evolutionary constraint.

Guess what? That’s exactly what they do see.

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Temporal expression divergence is minimized during the phylotypic period. a, Temporal divergence of gene expression at individual time points during embryogenesis. The curve is a second-order polynomial that fits best to the divergence data. Embryo images are three-dimensional renderings of time-lapse embryonic development of D. melanogaster using Selective Plane Illumination Microscopy (SPIM).

That trough in the graph represents a period of reduced gene expression variance between the species, and it corresponds to that phylotypic period. This is an independent confirmation of the morphological evidence: the similarities are real and they are an aspect of a conserved developmental program.

By the way, this pattern only emerges in developmental genes. They also examined genes involved in the immune system and metabolism, for instance, and they show no such correlation. This isn’t just a quirk of some functional constraint on general gene expression at one stage of development, but realy is something special about a developmental and evolutionary constraint.

The second paper by Domazet-Loso and Tautz takes a completely different approach. They examine the array of genes expressed at different times in embryonic development of the zebrafish, and then use a comparative analysis of the sequences of those genes against the sequences of genes from the genomic databases to assign a phylogenetic age to them. They call this phylostratigraphy. Each gene can be dated to the time of its origin, and then we can ask when phylogenetically old genes tend to be expressed during development.

The prediction here is that there would be a core of ancient, conserved genes that are important in establishing the body plan, and that they would be expressed during the phylotypic stage. The divergence at earlier and later stages would be a consequence of more novel genes.

Can you guess what they saw? Yeah, this is getting predictable. The observed pattern fits the prediction.

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(Click for larger image)

Transcriptome age profiles for the zebrafish ontogeny. a, Cumulative transcriptome age index (TAI) for the different developmental stages. The pink shaded area represents the presumptive phylotypic phase in vertebrates. The overall pattern is significant by repeated measures ANOVA (P = 2.4 3 10-15, after Greenhouse-Geisser correction P = 0.024). Grey shaded areas represent ± the standard error of TAI estimated by bootstrap analysis.

So what does this all tell us? That the phylotypic stage can be observed and measured quantitatively using several different techniques; that it represents a conserved pattern of development gene expression; and that the genes involved are phylogenetically old (as we’d expect if they are conserved.)

Domazet-Loso and Tautz propose two alternative explanations for the phenomenon, one of which I don’t find credible.

Adaptations are expected to occur primarily in response to altered ecological conditions. Juvenile and adults interact much more with ecological factors than embryos, which may even be a cause for fast postzygotic isolation. Similarly, the zygote may also react to environmental constraints, for example, via the amount of yolk provided in the egg. In contrast, mid-embryonic stages around the phylotypic phase are normally not in direct contact with the environment and are therefore less likely to be subject to ecological adaptations and evolutionary change. As already suggested by Darwin, this alone could explain the lowered morphological divergence of early ontogenetic stages compared to adults, which would obviate the need to invoke particular constraints. Alternatively, the constraint hypothesis would suggest that it is difficult for newly evolved genes to become recruited to strongly connected regulatory networks.

They propose two alternatives, that the phylotypic stage is privileged and therefore isn’t being shaped by selection, or that it is constrained by the presence of a complicated gene network, and therefore is limited in the amount of change that can be tolerated. The first explanation doesn’t make sense to me: if a system is freed from selection, then it ought to diverge more rapidly, not less. I’m also baffled by the suggestion that the mid-stage embryos are not in direct contact with the environment. Of course they are…it’s just possible that that mid-development environment is more stable and more conserved itself.

What we need to know more about is the specifics of the full regulatory network. A map of the full circuitry, rather than just aggregate measures of divergence, would be nice. I’m looking forward to it!

The creationists aren’t, though.

Domazet-Loso, T., & Tautz, D. (2010). A phylogenetically based transcriptome age index mirrors ontogenetic divergence patterns. Nature 468 (7325): 815-818. DOI: 10.1038/nature09632

Kalinka, A., Varga, K., Gerrard, D., Preibisch, S., Corcoran, D., Jarrells, J., Ohler, U., Bergman, C., Tomancak, P. (2010). Gene expression divergence recapitulates the developmental hourglass model. Nature 468 (7325): 811-814 DOI: 10.1038/nature09634

My mouse has two daddies

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This is awesome news. Biologists have figured out how to enable two male mice to have babies together, with no genetic contribution from a female mouse. I, for one, look forward to our future gay rodent overlords.

It was a clever piece of work. Getting progeny from two male parents has a couple of difficulties. One is that you need an oocyte, which is a large, specialized, complex cell type, and males don’t make them. Not at all. You can tear a boy mouse to pieces looking for one, and you won’t find a single example—they’re a cell found exclusively in female ovaries.

Now you might think that all we’d have to do is grab one from a female mouse, throw out its nuclear contents, and inject a male nucleus into it, but that doesn’t work, either. The second problem is that during the maturation of the oocyte, the DNA has to be imprinted, that is, given a female-specific pattern of activation and inactivation of genes. If that isn’t done, there will be a genetic imbalance at fertilization, and development will be abnormal. What we need to be able to do is grow an oocyte progenitor with male DNA in a female ovary.

So that’s what was done, and here’s how.

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Start with Father #1, whose cells all contain an X and a Y chromosome. Connective tissue cells were extracted from the mouse (in this case, an embryo), and then reprogrammed by viral transduction with modified copies of the genes Pou5f1, Sox2, Klf4, and Myc. This step produces induced pluripotent stem cells (iPS cells), or cells that have the ability to develop into all (probably) of the tissues of the body. These cells are then grown in a dish.

The next step is to give Father #1’s cells a sex change operation. This turns out to be trivial: in culture, cells can spontaneously lose a chromosome by non-disjunction, and 1-3% of the cells will lose their Y chromosome, and convert to X0. No Y chromosome means it is now a functionally female cell.

There is a significant difference between humans and mice here. Sometimes (about 1 in 5,000 births) humans are born with only one X chromosome, a condition called Turner syndrome. These individuals appear to be entirely normal females, except for some minor cosmetic differences, an unfortunate predisposition to a few problems like heart disease, and of particular relevance here, are also sterile. Mice are different: Turner syndrome mice are fertile. Apparently, mice have a god-given edge in the gay reproduction race.

Once a population of Father #1’s cells that are X0 are identified, they are then injected into a female mouse blastocyst to produce a chimera, an embryo with a mix of host cells (which are genetically XX) and donor cells (which are X0). That they’re mixed together in the resulting offspring doesn’t matter; it may be a callous way of looking at it, but the only purpose of the host XX cells is to provide a female mouse environment to house Father #1’s X0 cells that end up in the ovaries.

That’s the result of all this tinkering: a female mouse is born with a subset of Father #1’s reprogrammed cells nestled in her ovaries, where they mature in a female body and differentiate into oocytes. The oocytes divide by meiosis, producing egg cells that contain either one X chromosome, or no sex chromosome at all (0).

Finally, Father #2 comes into the picture. Father #2 is an ordinary male, with testes containing cells that go through meiosis and mature into ordinary sperm containing either one X chromosome or one Y chromosome. These sperm are used to fertilize eggs from the chimeric female, which, by all the shenanigans describe above, are derived from Father #1. Both male (XY) and female (X0) progeny ensue. That this actually occurred was thoroughly confirmed by testing the progeny for genetic markers from both fathers…and it’s true. The only genetic contributions were from the dads, and nothing from the host mother.

Now you may be sitting at home with your dearly beloved gay partner and wondering whether you will be able to have babies together someday. Or perhaps you’re a narcissistic man sitting at home alone, thinking you’d like to have babies with yourself, if only you could convince a few of your cells to make eggs (this is another possibility: there is no barrier to this technique being applied in cases where Father #1 is also Father #2, except that it is incestuous to the max). I expect it will be possible someday, but it isn’t right now. There are a few obstacles to doing this in humans.

  1. We haven’t worked out that genetic reprogramming trick for humans yet, so we don’t have a technique for producing pluripotent stem cells from your somatic cells. Give it time, though, and keep funding adult stem cell research, and it’ll happen.

    Also note the rule of unintended consequences. The fundy fanatics have been anti-embryonic stem cell research for years, and one of their tactics has been to insist that adult stem cell research is far more important. In the long run, it is…and oh, look what we’ll be able to do!

  2. The reprogramming trick involves viral transfection, the insertion of mutant copies of a few specific genes. This is probably not desirable. All kids are mutant anyway, but this is adding a specific, constant kind of mutation to all of the individuals produced by this method.

  3. It still requires a woman, and a woman who has been embryonically modified as a blastocyst at that. Did you know women have rights, including the right to not be a vessel for a scientific experiment? It’s true. They also take years and years to grow to sexual maturity, so even if you got started right now it would be a dozen years before she started making oocytes for you, and by the way, she’d inform you that she only produces eggs for herself, not you.

    There may be ways around this, but the techniques aren’t here yet. To produce eggs, we really don’t need the whole woman, just the ovary: another goal of stem cell research is to regrow organs from cells in a dish, for instance to build a new heart or pancreas for transplantation. Consider ovaries on the list of organs.

  4. That difference between mice and humans, that X0 mice are fertile while X0 women are not, seems like a serious problem. We apparently need the pair of X chromosomes working together to provide the correct gene dosage for normal maturation of the egg. It just means that we need to add an extra step to the procedure for people, though: transfer by injection an extra X chromosome from a donor cell from Father #1 to the X0 cells, producing a composite XX cell derived entirely from a male.

  5. The fundies will go raving apeshit bonkers. So what else is new?

  6. OK, there are also some serious ethical concerns that would need to be worked out, independent of the Bible-thumping theocratic sex police. As you can see from the recipe above, this is a procedure that involves extensive manipulation of embryos, almost all of it experimental, and the end result is…a baby. We should be conscientious in our care in any procedure that can produce human beings, especially if there is risk of producing damaged human beings. This can also only be categorized as a kind of expensive luxury treatment, and it’s difficult to justify such elaborate work for solely egotistical gratification. Especially for you, nerd-boy masturbating alone at home. (But learning more about the mechanisms of reproduction is more than enough to justify this work in mice, at least).

Wait…all this is just for male gay couples. What about nurturing lesbians who want to have children together? That has another tricky problem: you need a Y chromosome to induce normal sperm differentiation, and lesbian couples don’t have any of those. At all. They’re going to have to go to a male donor for a genetic contribution, diluting the purity of the genetic side of the procedure. However, that has a technology in the works to help out already: see obstacle #4 above. We’ll have to isolate iPS cells from Mother #1, inject a donor Y chromosome into them, cultivate chimeric male (or chimeric testis in a dish) to produce sperm, and then fertilize eggs from Mother #2 with the Mother #1-derived sperm. Any sons produced by this procedure would have three parents, Mother #1, Mother #2, and the Male Donor who provided the Y chromosome, and only the Y chromosome. Any daughters, though, would only have two parents: Mother #1 and Mother #2.

Isn’t reproductive biology fun? It’s the combination of exciting science with terrifyingly deep social implications.

Deng JM, Satoh K, Chang H, Zhang Z, Stewart MD, Wang H, Cooney AJ, Behringer RR (2010) Generation of viable male and female mice from two fathers. Biology of Reproduction DOI:10.1095/biolreprod.110.088831.

Student biologists blogging some more

You all want to know what is going on in the minds of my students, right? Here you go.

More scenes from the minds of my students

My developmental class is still plugging away with some new entries.

A surprising Nobel

I would never have guessed this one. The Nobel Prize in Medicine has gone to Robert G. Edwards for his pioneering work in in vitro fertilization. It surprises me because it’s almost ancient history — he is being rewarded for work done over 30 years ago. It’s also very applied research — this was not work that greatly advanced our understanding of basic phenomena in biology, because IVF was already being done in animals. This was just the extension of a technique to one peculiar species, ours.

I don’t begrudge him the award, though, because the other special property of his research was that it was extremely controversial. These were procedures that simply burned through scores (or hundreds, if you count the ones with such little viability that they weren’t implanted) of human zygotes in order to work out reliable protocols, and throughout faced serious ethical risks — these were procedures that had a chance of producing the worst possible result, a viable embryo that came to full term, but had serious birth defects. The public opposition to the work was tremendous, funding was tenuous, and even many in the scientific community opposed the work and ostracized Edwards and his colleague, Steptoe (who did not live to see this day, and so did not receive the award).

Nowadays, IVF is practically routine and about 4 million people were ‘test tube babies’. It’s still controversial, though, with extremist anti-abortion groups, such as the Catholic church, still fighting it, and the redundant, unused zygotes from the procedure still being a point of major contention (ever heard of ‘snowflake babies’? That’s what they’re talking about).

I’m reading a couple of messages in this award. One is simply acknowledging a hard-working scientist, but the other is a signal that we should soldier on through all of the opposition to reproductive health technologies, that science will be rewarded and the Luddites will find themselves in the dustbin of history. I can’t help but see this as, in part, the Nobel committee making an unmistakeably rude gesture at the anti-science, anti-choice fanatics of the religious right.

(For those who are unfamilar with the IVF procedure that Edwards and Steptoe developed, here’s a lovely summary diagram from the Nobel Foundation.)

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The class writes

I told you I’ve got my development class blogging, and here’s the update for this week.

Don’t be shy. They’ve been told to welcome comments and to brace themselves for possible criticisms.

We teach developmental biology at UMM

I’m back to teaching developmental biology this term, and one of the things I do in my upper level classes is have students write blog entries on the themes of the course. In the past, I’ve given them space right here to do that, which I’ve found to be a parlous course of action — the commentariat here is savage and brutal, and infested with trollish nitwits who can derail threads spectacularly, so I’m doing it a little differently this time around. I’ve had them create their very own blogs on their own spaces, which has the additional benefit that maybe they can keep them going after they graduate.

So here’s the list of student blogs from my course. Feel free to visit, criticize, comment, etc., but do remember that they’re just now learning, so constructive discussion is far better than our usual ravaging ferocity. They’ve also been warned to be thick-skinned, though, so you don’t have to be too gentle.

Developmental Biology blogs

There isn’t much there yet in most cases, since they’ve just set them up, but I’ll be making weekly links to relevant articles in the future.

While I’m at it, I’ll mention that a former student, Levi Simonson, has a blog from his perspective as an ex-UMM student, now a graduate student at the wonderful University of Oregon. People do leave here to go on to interesting work!

Beehive development

A beekeeper did something simple: he put a bell jar over an opening in his beehive. The bees obliged by building a hive within it, where you could see it, and captured the process in a series of photos.

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I’m fascinated by the fact that the first struts in the framework are regularly spaced vertical bars of wax — how did they do that? I want to see videos of those early stages when the bees are working to initiate the strips. I suspect there are some interesting bee:bee interactions going on as they set them up.