SciAm explains hothead

You may have heard about that odd hothead mutation in Arabidopsis that seemed to be violating a few principles of basic genetics—there was an unexpectedly high frequency of revertants that suggested there might be a reservoir of conserved genetic information outside the genome. Reed Cartwright proposed an alternative explanation, that gamete selection could skew the results. Now the latest reports suggest that the bias was an artifact of foreign pollenization (which I think is interesting in itself. Life is damned good at sneaking its genes in wherever it can.)

Anyway, if that’s all gobbledygook to you, Scientific American has put up a lucid summary of the hothead affair. It’s an example of good science, where the observations and hypotheses are hammered out and refined to get a best explanation.

Evolution of sensory signaling

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How we sense the world has, ultimately, a cellular and molecular basis. We have these big brains that do amazingly sophisticated processing to interpret the flood of sensory information pouring in through our eyes, our skin, our ears, our noses…but when it gets right down to it, the proximate cause is the arrival of some chemical or mechanical or energetic stimulus at a cell, which then transforms the impact of the external world into ionic and electrical and chemical changes. This is a process called sensory signaling, or sensory signal transduction.

While we have multiple sensory modalities, with thousands of different specificities, many of them have a common core. We detect both light and odor (and our cells also sense neurotransmitters) with similar proteins: they use a family of G-protein-linked receptors. What that means is that the sensory stimulus is received by a receptor molecule specific for that stimulus, which then actives a G-protein on the intracellular side of the cell membrane, which in turn activates an effector enzyme that modifies the concentration of second messenger molecules in the cell. Receptors vary—you have a different receptor for each molecule you can smell. The effector enzymes vary—it can be adenylate cyclase, which changes the levels of cyclic AMP, or it can be phospholipase C, which generates other signalling molecules, DAG and IP3. The G-protein that links receptor and effector is the common element that unites a whole battery of senses. The evolutionary roots of our ability to see light and taste sugar are all tied together.

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And the Nobel goes to…

Andrew Fire and Craig Mello, for the discovery of RNAi. Read Pure Pedantry for an explanation for why this is important.

I’ll also mention that Carl Zimmer presents his take on this award…and wouldn’t you know it, evolution has its greasy fingerprints all over it.

I must also promote an excellent comment from Andy Groves:

I’ve said it before, and I’ll say it again for the benefit of ID supporters out there – this is what a real scientific revolution looks like. Fire and Mello published their paper in 1998 (two years after “Darwin’s Black Box” came out, for those who are interested). Since then, the number of primary research papers on RNAi, siRNAs and miRNAs stands at 12399, using the search terms

(RNAi OR siRNA OR miRNA) NOT review

12400 papers in eight years. That’s 1550 a year, or just over four papers a day. Would Bill Dembski, the Isaac Newton of information theory, care to comment?

Hmmm?

Every science paper, every bit of recognition given to working scientists, seems to be a rather nasty rebuke to the promulgators of creationism.

The Morris Café Scientifique lurches to life again!

Once again this year, I’m setting up our Café Scientifique-Morris, which is going to be held on the last Tuesday of each month of the university school year. This time around, that means the first one falls on…Halloween! So we’re going to do something fun for that one: maybe some costumes, lots of clips from classic horror movies, I definitely think we’re going to need some bubbling retorts of colored fluids, and the chemistry department is tentatively going to provide some treats (ice cream made with liquid nitrogen—chemistry and treats don’t usually go together in people’s heads, I know.) This is the announcement for the first talk:

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I’ve been ripping a few DVDs from my collection with classic portrayals of scientists—the Universal Frankenstein series, Re-animator, the Bond movies, etc. (any suggestions? Pass ’em on)—which show us off as evil villains, and I’m going to show short clips from them to illustrate our poor image. Then I’m going to follow up with more but less exciting clips of people like Sagan and Wilson and Dawkins and, if I can track it down, Bronowski to illustrate the real humanism of good scientists. Suggestions for the latter part are also welcome, and that will be the heart of the talk, but face it: I don’t want to overdo the moralizing, and all the fun is going to be in the monster-makers.

I’ve also finalized our schedule. I’ve opened it up to a few people on the other side of campus, so we’re also going to hear about the legal standards for the admission of scientific evidence, and the economics of alternative power generation and transmission, in addition to a discussion of the chemistry we all use in our homes, a bit of astronomy, and a session of insect identification.

  • 31 October 2006 :: PZ Myers, Biology
  • 28 November 2006 :: Theodora Economou, Law
  • 30 January 2007 :: Panel discussion, Chemistry
  • 27 February 2007 :: Arne Kildegaard, Economics
  • 27 March 2007 :: Kristin Kearns, Physics
  • 24 April 2007 :: Tracey Anderson, Biology

It’s looking like a good year for this seminar series. If you’re in the neighborhood, stop on by!

Hox complexity

Here’s a prediction for you: the image below is going to appear in a lot of textbooks in the near future.

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Confocal image of septuple in situ hybridization exhibiting the spatial expression of Hox gene transcripts in a developing Drosophila embryo. Stage 11 germband extended embryo (anterior to the left) is stained for labial (lab), Deformed (Dfd), Sex combs reduced (Scr), Antennapedia (Antp), Ultrabithorax (Ubx), abdominal-A (abd-A), Abdominal-B (Abd-B). Their orthologous relationships to vertebrate Hox homology groups are indicated below each gene.

That’s a technical tour-de-force: it’s a confocal image of a Drosophila embryo, stained with 7 fluorescent probes against different Hox genes. You can clearly see how they are laid out in order from the head end (at the left) to the tail end (which extends to the right, and then jackknifes over the top). Canonically, that order of expression along the body axis corresponds to the order of the genes in a cluster on the DNA, a property called colinearity. I’ve recently described work that shows that, in some organisms, colinearity breaks down. That colinearity seems to be a consequence of a primitive pattern of regulation that coupled the timing of development to the spatial arrangements of the tissues, and many organisms have evolved more sophisticated control of these patterning genes, making the old regulators obsolete…and allowing the clusters to break up without extreme consequences to the animal. A new review in Science by Lemons and McGinnis that surveys Hox gene clusters in different lineages shows that the control of the Hox genes is much, much more complicated than previously thought.

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Cellular responses to alcohol

Forgive me, but I’ll inflict a few more zebrafish videos on you. YouTube makes this fun and easy, and I’m going to be giving my students instruction in video micrography next week, so it’s good practice.

This is a more detailed look at what’s going on in the embryo. Using a 40x objective, we zoom in on a patch of cells near the surface of a 4-hour-old embryo—this is a generic tissue called the blastoderm. We just record activity with an 1800-fold time compression for a few hours to see what the cells are doing. The movie below displays typical, baseline activity: the cells are jostling about, you’ll see an occasional mitosis, and sometimes you’ll see a cell vanish out of focus as it moves deeper into the embryo, and sometimes you’ll suddenly see a new cell squirm to the surface. It’s all just a happy, dynamic place with lots of random motion; these can be mesmerizing to watch.

These blastoderm sheets are a kind of cellular testbed for quick assays of the effects of teratogens on embryonic tissues. We just wash the embryo with whatever substance we’re interested in testing, and see if and how the cells react.

Alcohol is a dramatic example. Here’s a blastoderm sheet under stress as it is exposed to 3% ethanol.

Some obvious changes are going on. One is that the surfaces of the individual cells are seething—they are bubbling out and sucking back in little balloons of membrane, a process called blebbing. This is a very typical response to any kind of stress. Apparently, mitosis is another kind of stress: we can reduce the concentration of alcohol so that the cells look normal, except that as they’re about to divide they go into a flurry of blebbing that persists until division is complete.

We had another puzzle to solve. Sometimes, as we were looking at our low magnification recordings of embryos, we’d see the whole blastula or gastrula shudder. They don’t have muscles yet! We didn’t know what was causing pulses of contractile activity to sweep across the whole animal at such a relatively undifferentiated stage.

These movies show what was going on. They’re a real pain to keep in focus, because in addition to the fine blebbing activity in individual cells, the whole surface occasionally dimples and changes shape. What’s happening? Cells are dying somewhat randomly, some on the surface, some deeper in the embryo. Deep cells that die seem to be actively evicted from interior; sometimes the surface will buckle inward (with the image going out of focus), and when it bounces back up, it ejects a load of cellular debris out into the external medium. There’s a particularly dramatic example at the end of this movie, where everything in the lower half goes massively out of focus, and when it bounces back, it carries a large dead cell that sits there briefly, then abruptly pops and disappears.

If you look at that earlier lower resolution movie of ethanol effects, you might notice odd rough blobs on the surface of the embryo, and we think what that is is the extruded debris of deep cells killed by alcohol exposure, thrown up out of the interior to prevent them from interfering with normal development. This is actually a rather cool cellular mechanism that helps embryos survive random glitches in the process of building these massive pools of cells as it grows—it’s a kind of tissue-level garbage disposal service.