Evolution of vertebrate eyes

Blogging on Peer-Reviewed Research

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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Blogging on Peer-Reviewed Research

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?

Blogging on Peer-Reviewed Research

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

Blogging on Peer-Reviewed Research

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.

Sad case out of India

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What do you do when a child is born with ischiopagus?

  1. Sell her to the circus?

  2. Turn her into an object of religious veneration?

  3. Try surgery to correct the condition as much as possible?

This little girl born with six legs and two arms had the option of all three; she’s currently being operated on to remove four of the limbs. I don’t think it is an easy decision, except for the fact that her condition is messed up enough that she’s not likely to survive to adulthood without the surgery. On the complicating side, the operation costs £100,000, has substantial risk of death or paralysis, and will not restore full, normal morphology. Here’s a paper describing the long term outcome of another case of a separation of conjoined twins.

Because we can’t rewind the clock, developmental abnormalities often are not correctable—they are treatable, which is a whole different thing, but the doctors can’t change the fact that this child is the result of a scrambled developmental process.

I stand corrected. The two medial posterior limbs are arms, so this is a conjoined twin with four arms and four legs, and with the second twin headless.

Once more into the Haeckelian morass; or, Peter Moore is an illiterate fool

Perhaps you haven’t noticed, but we’ve got a serial spammer in the comments. This twit, calling himself Peter Moore (also known as Ken DeMyer, or Kdbuffalo, as he was known on Wikipedia before being banned there), is repeating himself over and over again, asking the same stupid question, never satisfied with any answer anyone gives him. Forty nine insipid comments in three days is enough.

I will answer him one last time. Any further attempt to spam multiple comment threads with his demands (and this alone makes him an ass: an incompetent, unqualified hack like Moore is in no position to make demands) will result in his immediate banning.

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Nobel in Medicine goes to…

I’ve known for years that this was going to happen: Mario Capecchi, Oliver Smithies and Briton Martin Evans have won the Nobel Prize in Medicine for their work on targeted gene mutations. If you’re interested in what kinds of work they’ve done, I described one paper on Hox regulatory evolution, and this work on the evolution of the Hox code wouldn’t have been possible without their knockout techniques.