Coyne is on the Loom

We had Neil Shubin here last week, and now Jerry Coyne is guest-blogging at The Loom. I look forward to the day that I can just sit back and invite prominent scientists to do my work for me here.

Although, I have to say that while Coyne is largely correct, he’s being a bit unfair. He’s addressing Olivia Judson’s recent article on “hopeful monsters”, a concept Coyne and the majority of the biological community reject. I reject it, too, but I think there are some legitimate issues that are associated with the idea that are also all too often and unfortunately discarded.

One point that Coyne handles well: there is a disconnect between the magnitude of genotypic changes and phenotypic effects — a single point mutation can cause amazing morphological changes. As Coyne points out, though, although this can happen, it’s not likely to be a major force in evolutionary change. Dramatic, single-step phenotypic effects are the kinds of things that geneticists select for, but they are also exactly the kinds of things that nature selects against. Evolution is much more likely to sidle up towards a major change by successive smaller steps, since those small changes are less likely to be accompanied by major deleterious side effects. Also, phenotypic outcomes of development should be robust to be advantageous, which typically means that there are many regulatory events cooperating to produce them — and they are therefore buffered by multiple controls.

But please, let’s not always dismiss Richard Goldschmidt when discussing “hopeful monsters”. It really wasn’t that awful an idea. Goldschmidt worked on stable variations in organisms: he studied sex differences (ever noticed that males and females have pretty much the same genes, but different phenotypes?) and metamorphosis (similarly, an organism builds two or more very different morphologies with exactly the same genome). He postulated that there could be specific, well-structured, stable nodes of patterns of gene expression — genes weren’t generally fluid, but tended to lock in to particular states. If he were writing today, he’d probably be bringing up the notion of attractors in chaos theory; the ideas are very similar. In that context, he was proposing a worthy concept that should have been taken more seriously than it was — Mayr’s hatchet job was particularly awful.

The “hopeful monster” concept was not shot down by the synthesis — it was ignored. I think it’s been dismantled by developmental biology, though; what we’ve learned is that the stable morphological types we see in a single species are not simply fortunate stable nodes in a nucleus that can be tuned in different ways, but that each are the product of many generations of slow sculpting by the processes of evolution, and that they are riddled with clumsy kluges that aren’t the outcome of some elegant global pattern switching mechanism, but of a long history of small tweaks.

Now also, Coyne is no fan of evo-devo, and he briefly voices the suggestion that the evolutionary developmental biologists are among the sources of this idea that saltational changes lead to sudden, drastic changes in body plans … but I’m just not seeing that. I am seeing work, for instance, that suggests that Hox duplications have been part of the process of producing additions to body plans, but it’s not a case of “poof, arthropods gain a metathorax in one change” — it’s been quite conventional. It’s more like “poof, arthropods gain an extra Hox gene, which initially adds redundancy and is later shaped by evolutionary processes that confer additional specializations on a segment,” quite ordinary stuff that shouldn’t be at all objectionable to Coyne.

It’s especially peculiar to pin the “hopeful monster” concept on evo-devo, when the one evo-devo expert he quotes, the biologist Sean Carroll, explicitly points out that evo-devo doesn’t support it.

Coyne is also going to be speaking at an evo-devo symposium I’ll be attending in April — I’m going to be very interested to hear what he has to say.

Where do the hagfish fit in?

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Hagfish are wonderful, beautiful, interesting animals. They are particularly attractive to evolutionary biologists because they have some very suggestive features that look primitive: they have no jaws, and they have no pectoral girdle or paired pectoral fins. They have very poorly developed eyes, no epiphysis, and only one semicircular canal; lampreys, while also lacking jaws, at least have good eyes and two semicircular canals. How hagfish fit into the evolutionary tree is still an open question, however.

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Neurulation in zebrafish

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Neurulation is a series of cell movements and shape changes, inductive interactions, and changes in gene expression that partitions tissues into a discrete neural tube. It is one of those early and significant morphogenetic events that define an important tissue, in this case the nervous system, and it’s also an event that can easily go wrong, producing relatively common birth defects like holoprosencephaly and spina bifida. Neurulation has been a somewhat messy phenomenon for comparative embryology, too, because there are not only subtle differences between different vertebrate lineages in precisely how they segregate the neural tissue, but there are also differences along the rostrocaudal axis of an individual organism. A recent review by Lowery and Sive, though, tidies up the confusion and pulls disparate stories together.

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Evolution of vertebrate eyes

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A while back, I summarized a review of the evolution of eyes across the whole of the metazoa — it doesn’t matter whether we’re looking at flies or jellyfish or salmon or shrimp, when you get right down to the biochemistry and cell biology of photoreception, the common ancestry of the visual system is apparent. Vision evolved in the pre-Cambrian, and we have all inherited the same basic machinery — since then, we’ve mainly been elaborating, refining, and randomly varying the structures that add functionality to the eye.

Now there’s a new and wonderfully comprehensive review of the evolution of eyes in one specific lineage, the vertebrates. The message is that, once again, all the heavy lifting, the evolution of a muscled eyeball with a lens and retinal circuitry, was accomplished early, between 550 and 500 million years ago. Most of what biology has been doing since is tweaking — significant tweaking, I’m sure, but the differences between a lamprey eye and our eyes are in the details, not the overall structure.

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Load-bearing adaptation of women’s spines

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Those of you who have been pregnant, or have been a partner to someone who has been pregnant, are familiar with one among many common consequences: lower back pain. It’s not surprising—pregnant women are carrying this low-slung 7kg (15lb) weight, and the closest we males can come to the experience would be pressing a bowling ball to our bellybutton and hauling it around with us everywhere we go. This is the kind of load that can put someone seriously out of balance, and one way we compensate for a forward-projecting load is to increase the curvature of our spines (especially the lumbar spine, or lower back), and throw our shoulders back to move our center of mass (COM) back.

Here’s the interesting part: women have changed the shape of individual vertebrae to better enable maintenance of this increased curvature, called lordosis, and fossil australopithecines show a similar variation.

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Evo-devo in 60 seconds

Here’s a useful excercise: can you summarize a key concept in your field in less than a minute? Chris Mims takes a stab at explaining evo-devo — he’s not trying to explain the whole field, actually, but the central concept of a master gene. He uses the analogy of a power strip for a transcription factor, which I like quite a bit, and I’m probably going to have to steal it someday.

What does it take to turn a stem cell into a cure?

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Last week, I reported on this new breakthrough in stem cell research, in which scientists have discovered how to trigger the stem cell state in adult somatic cells, like skin cells, producing an induced stem cell, a pluripotent cell that can then be lead down the path to any of a multitude of useful tissue types. I tried to get across the message that this is not the end of embryonic stem cell (ESC) research: the work required ESCs to be developed, the technique being used is unsuitable for therapeutic stem cell work, and there’s a long, long road to follow before we actually have stem cell “cures” in hand. A review on LiveScience emphasized similar reservations. Seizing on this one result as an excuse to end research on ESCs would be a great mistake.

So let’s consider what it takes to turn a stem cell into a medically useful tool. One “simple” (we’ll quickly see that it is anything but) example is finding a cure for type 1 diabetes. We understand that problem very well: people with this disease have lost one specific cell type, the β cells of the pancreas, which manufacture insulin. That’s all we have to do: grow up a dish full of just one cell type, the β cells, and plant them back in the patient’s gut, and presto, no more diabetes (setting aside the chronic difficulty of removing whatever destroyed the patient’s original set of β cells, that is). Sounds easy. It’s not.

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Stem cell breakthrough

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A recent discovery in stem cell research is no minor event: researchers have figured out how to reprogram adult cells into a state that is nearly indistinguishable from that of embryonic, pluripotent stem cells. This is huge news that promises to accelerate the pace of research in the field.

The problem has always been that cells exist in distinct states. A skin cell, for instance, has one set of genes essential for its specific function activated, and other sets of genes turned off; an egg cell has different patterns of gene activation and inactivation. Just taking the DNA from a skin cell and inserting it into the egg cell isn’t necessarily going to create a functional egg cell, because genes essential for egg cells may be switched off in the skin cell DNA, and we don’t know how to specifically switch them on. The process of somatic cell nuclear transfer has been hit or miss for that reason, with very high failure rates—scientists are basically trying to make the right configuration of genes switch on by giving the nucleus a good hard kick, and hoping that something in the cells will reconfigure the pattern of gene activation into something appropriate.

What the discovery by Takahashi et al. accomplishes is to reveal how to specifically switch on the right pattern of genes for a pluripotent stem cell. They have discovered the reset button for mammalian cells: a simple trigger that puts the cells in the right state to become anything else.

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Beaten to the vulva

Scooped! I’ve long adored vulvas, having written a few things on how to develop a vulva and how to evolve a vulva, so I’m a little peeved that this upstart at scienceblogs, Greg Laden, has written up a recent story on nematode vulva evolution before me. Aaargh, all vulvas must be mine! I’ve just got too much other work stacked in front of me.

I may have to revisit this story later, though. I made a quick skim of the paper and don’t see quite how they arrived at their conclusion, that vulva evolution is dominated by selective events rather than chance. I can’t say they’re wrong, but I’m going to have to read it more carefully before I can agree with it.