Crawling pigments

Here’s another of Casey Dunn’s Creature Casts, this time on shifting color spots in marine snails.

CreatureCast – Flamingo Tongue Snails from Casey Dunn on Vimeo.

Pigment cells are always very, very cool. I’ve been intrigued by them for a long time — they show up in my time-lapse recordings of developing zebrafish and are always active. Here’s a quick one, a few hours of time in a roughly 24 hour old zebrafish embryo, compressed to about 30 seconds. You can see one corner of the dark eye at the bottom left of the image, and that oval structure near the middle with two spots in it is the ear and its otoliths. The melanocytes are writhing over the side of the head and down onto the yolk sac; they’re not quite as colorful as the snail, but then, the zebrafish is a mostly black and white animal.

α-actinin evolution in humans

i-e88a953e59c2ce6c5e2ac4568c7f0c36-rb.png

Perhaps your idea of the traditional holiday week involves lounging about with a full belly watching football — not me, though. I think if I did, I’d be eyeing those muscular fellows with thoughts of muscle biopsies and analyses of the frequency of α-actinin variants in their population vs. the population of national recliner inhabitants. I’m sure there’s an interesting story there.

In case you’re wondering what α-actinin is, it’s a cytoskeletal protein that’s important in anchoring and coordinating the thin filaments of actin that criss-cross throughout your cells. It’s very important in muscle, where it’s localized in the Z-disk at the boundaries of sarcomeres, the repeated contractile units of the muscle. This diagram might help you visualize it:

i-60cbd272718c8f724ef1452d79d99d6a-sarcomere.jpeg
Actin (green), myosin (red). Rod-like tropomyosin molecules (black lines). Thin filaments in muscle sarcomeres are anchored at the Z-disk by the cross-linking protein α-actinin (gold) and are capped by CapZ (pink squares). The thin-filament pointed ends terminate within the A band, are capped by tropomodulin (bright red). Myosin-binding-protein C (MyBP-C; yellow transverse lines).

The most prominent elements in the picture are the thin filaments (made of actin) and thick filaments (made of myosin) which slide past each other, driven by motor proteins, to cause contraction and relaxation of the muscle. The α-actinin proteins are the subtle orange lines in the Z disks on the left and right.

The α-actinin proteins are evolutionarily interesting. In vertebrates, there are usually four different kinds: α-actinin 1, 2, 3, and 4. 1 and 4 are ubiquitous in all cells, since all cells have a cytoskeleton, and the α-actinins are important in anchoring the cytoskeleton. α-actinin-2 and -3 are the ones of interest here, because they are specifically muscle actinins. α-actinin-2 is found in all skeletal muscle fibers, cardiac muscle, and also in the brain (no, not muscle in the brain, there isn’t any: in the cytoskeleton of neurons). Just to complicate matters a bit, α-actinin-2 is also differently spliced in different tissues, producing a couple of isoforms from a single gene. α-actinin-3 is not found in the brain or heart, but only in skeletal muscle and specifically in type II fast glycolytic muscle fibers.

Muscle fibers are specialized. Some are small diameter, well vascularized, relatively slow fibers that are optimized for endurance; they can keep contracting over and over again for long periods of time. These are the fibers that make up the dark meat in your Christmas turkey or duck. Other fibers are large diameter, operate effectively anaerobically, and are optimized for generating lots of force rapidly, but they tend to fatigue quickly — and there are more of these in the white meat of your Christmas bird. (There are also intermediate fiber types that we won’t consider here.) Just keep these straight in your head to follow along: the fast type II muscle fibers are the ones that you use to generate explosive bursts of force, and may be enriched in α-actinin-3; the slower fibers are the ones you use to keep going when you run marathons, and contain α-actinin-2. (There are other even more important differences between fast and slow fibers, especially in myosin variants, so differences in α-actinins are not major determinants of muscle type.)

Wait, what about evolution? It turns out that invertebrates only have one kind of α-actinin, and vertebrates made their suite of four in the process of a pair of whole genome duplications. We made α-actinin-2 and -3 in a duplication event roughly 250-300 million years ago, at which time they would have been simple duplicates of each other, but they have diverged since then, producing subtle (and not entirely understood) functional differences from one another, in addition to acquiring different sites of expression. α-actinin-2 and -3 in humans are now about 80% identical in amino acid sequence. What has happened in these two genes is consistent with what we know about patterns of duplication and divergence.

i-75f72fe14fd19d142167119147ebce45-duplication.jpeg
Using sarcomeric α-actinin as an example, after duplication of a gene capable of multiple interactions/functions, there are two possible distinct scenarios besides gene loss. A: Sub-functionalisation, where one interaction site is optimised in each of the copies. B: Neo-functionalisation, where one copy retains the ancestral inter- action sites while the other is free to evolve new interaction sites.

So what we’re seeing in the vertebrate lineage is a conserved pattern of specialization of α-actinin-3 to work with fast muscle fibers — it’s a factor in enhancing performance in the specific task of generating force. The α-actinin-3 gene is an example of a duplicated gene becoming increasingly specialized for a particular role, with both changes in the amino acid sequence that promoted a more specialized activity, and changes in the regulatory region of the gene so that it was only switched on in appropriate muscle fibers.

i-e5ab4d9006f937a9907d72bd7ae1aac0-actn_history.jpeg
Duplication and divergence model proposed by this paper. Before duplication the ancestral sarcomeric α-actinin had the functions of both ACTN2 and ACTN3 in terms of tissue expression and functional isoforms. After duplication, ACTN2 has conserved most of the functions of the preduplicated gene, while ACTN3 has lost many of these functions, which may have allowed it to optimise function in fast fibres.

That’s cool, but what we need is an experiment: we need to knock out the gene and see what happens. Mutations in α-actinin-2 are bad—they cause a cardiomyopathy. Losing α-actinin-4 leads to serious kidney defects (that gene is expressed in kidney tissue). What happens if we lose α-actinin-3?

It turns out you may be a guinea pig in that great experiment. Humans acquired a mutation in the α-actinin-3 gene, called R577X, approximately 40-60,000 years ago, and this mutation is incredibly common: about 50% of individuals of European and Asian descent carry it, and about 10% of individuals from African populations. Furthermore, an analysis of the flanking DNA shows relatively little recombination or polymorphism — which implies that the allele has reached this high frequency relatively recently and rapidly, which in turn implies that there has been positive selection for a nonsense mutation that destroys α-actinin-3 in us. The data suggests that a selective sweep for this variant began in Asia about 33,000 years ago, and in Europe about 15,000 years ago.

There is no disease associated with the loss of α-actinin-3. It seems that α-actinin-2 steps up to the plate and fills the role in type II fast muscle fibers, so everything functions just fine. Except…well, there is an interesting statistical effect.

The presence of a functional α-actinin-3 gene is correlated with athletic performance. A study of the frequency of the R577X mutation in athletes and controls found that there is a significant reduction in the frequency of the mutation among sprinters and power-lifters. At the Olympic level, none of the sprinters in the sample (32 individuals) carried the α-actinin-3 deficiency. Among Olympic power lifters, all had at least one functional copy of α-actinin-3.

Awesome. Now I’m wondering about my α-actinin-3 genotype, and whether I have a good biological excuse for why I always got picked last for team sports in high school gym class. This is also why I’m interested in taking biopsies of football players…both for satisfying a scientific curiosity, and for revenge.

You may be wondering at this point about something: α-actinin-3 has a clear beneficial effect in enhancing athletic performance, and its conservation in other animal species suggests that it’s almost certainly a good and useful protein. So why has there been positive selection (probably) for a knock-out mutation in the human lineage?

There is a weak correlation in that study of athletic performance that high-ranking athletes in endurance sports have an increased frequency of the R577X genotype; it was only seen in female long-distance runners, though. More persuasive is the observation that α-actinin-3 knockouts in mice also produced a shift in metabolic enzyme markers that are indicative of increased endurance capacity. The positive advantage of losing α-actinin-3 may be more efficient aerobic metabolism in muscles, at the expense of sacrificing some strength at the high end of athletic performance.

This is yet another example of human evolution in progress—we’re seeing a shift in human muscle function over the course of a few tens of thousands of years.

Lek M, Quinlan KG, North KN (2009) The evolution of skeletal muscle performance: gene duplication and divergence of human sarcomeric alpha-actinins. Bioessays 32(1):17-25. [Epub ahead of print]

MacArthur DG, Seto JT, Raftery JM, Quinlan KG, Huttley GA, Hook JW, Lemckert FA, Kee AJ, Edwards MR, Berman Y, Hardeman EC, Gunning PW, Easteal S, Yang N, North KN (2007) Loss of ACTN3 gene function alters mouse muscle metabolism and shows evidence of positive selection in humans. Nat Genet.39(10):1261-5.

Yang N, MacArthur DG, Gulbin JP, Hahn AG, Beggs AH, Easteal S, North K (2003) ACTN3 genotype is associated with human elite athletic performance. Am J Hum Genet 73(3):627-31.

Evolving fish of the lower Congo

The lower Congo river is deep and complex, and there are a surprising number of hydrologic features that act as barriers separating populations of fish — this very nice video explains the diversity of species and the ongoing evolution of the fish in this environment.

They too briefly showed a blind depigmented cichlid that apparently lives in very deep troughs in the river — I wanted to see more about that. It’s probably out of the question to send divers down into that maelstrom, but cameras? Someday? Please?

Why climatologists used the tree-ring data ‘trick’

Since we’re arguing over global warming this week, I thought I’d post a commentary piece that was published in the Morris newspaper this week, by my colleague Pete Wyckoff. Pete is our local tree and climate expert, who works in both the biology and environmental studies discipline, and is very well qualified to describe what was going on with some of the adjustments in the climate data that have some of the nuts screaming shrilly on Fox News.

Local Commentary: Thoughts on ‘Climate-gate’: Mitigate our impact

By Pete Wyckoff

Is the planet cooling? “I’ve just completed Mike’s Nature trick…to hide the decline,” writes climate scientist Phil Jones in a stolen 1999 e-mail which has caused a frenzy. FoxNews.com tells us that we finally have a ‘smoking gun’–proof that scientists are manufacturing a global warming crisis so that they can… they can…(I’ve never really understood the goals of the evil scientific conspirators).

The planet is warming. The data are unequivocal and based on measured temperatures (corrected for things like the “heat island” effect, so please don’t write an angry response claiming that the thermometers are wrong). What Phil Jones was referring to is something else: past temperatures estimated via tree rings. Since 1960, the rings in trees seem to have lost some of their power to record temperature.

Why should tree rings indicate temperature at all? As most of us learned in childhood, the trunks of trees at our latitude tend to put on a distinct growth ring every year. All other things being equal, when the trees are happy, they put on a large ring. When the going gets tough, the rings get thin. What makes a tree happy? Light, nutrients, lack of disease, and warmth (to a point). What do trees despise? Drought. By careful interpretation of past tree growth patterns, we can learn a lot about past climates.

Scientists have spent many years developing the techniques needed to reconstruct climate via tree rings. The problem is that in the past few decades, the tree ring-climate relationships seem to have become “decoupled” in many areas. Why? The main cause seems to be increasing atmospheric carbon dioxide. While carbon dioxide is famously a gas that heats the planet (the greenhouse effect is real and uncontroversial), carbon dioxide also directly impacts plants. Carbon dioxide fuels photosynthesis, and increased carbon dioxide in the air can both speed-up plant growth and make plants less sensitive to drought.

Decreased drought sensitivity is an expected response for plants exposed to high levels of carbon dioxide. All along the underside of a plant’s leaves are little holes called “stomata.” These holes can open and close. A tree must open its stomata to take in carbon dioxide for photosynthesis. Unfortunately, plants lose water out of their open stomata. Plants growing in air that has lots of carbon dioxide can reduce the amount of time their stomata are open, thus making them lose less water and become less susceptible to drought.

Biologists call the concept here “water-use efficiency,” and it is of crucial interest to farmers and foresters alike. Carbon dioxide causes warming that will likely make west central Minnesota a drier place in the future. At the same time, increased carbon dioxide in the air makes plants growing in our region less susceptible to drought. The balance between these two forces will be crucial.

The changing relationship between climate and tree growth is a hot topic of research at your local university. Last Friday, Dr. Chris Cole and Dr. Jon Anderson, of the University of Minnesota, Morris, published a paper in the journal “Global Change Biology” showing that aspen trees in Wisconsin are growing faster than they used to, and much of the increase is attributed to increased atmospheric carbon dioxide. Two weeks ago, a former student and I published a paper in the “Journal of Ecology” showing that oak trees in west central Minnesota became less sensitive to drought during the 20th century. If “dust bowl”-severity droughts come again soon, we project that the local oaks will suffer 50 percent less mortality than they likely did in the 1930s.

So what does this all mean? The relationship between tree rings and climate is becoming muddied by the rapid recent increase in atmospheric carbon dioxide. For most of the past 10,000 years, carbon dioxide levels in the atmosphere remained reasonably stable. Now they are skyrocketing. Modern tree rings are no longer the reliable recorders of temperature they once were. It is a good thing that we now have thermometers.

What does Phil Jones’ stolen e-mail not mean? It does not mean that global warming is a hoax. It does not mean that there are really any cracks in the scientific consensus that humans are causing dangerous alterations to the global climate.

We humans are changing the climate, largely by emitting vast quantities of carbon dioxide via the way we heat our houses, fuel our cars, and generate our electricity. This is unwise. Yes, the future climate, along with the increased carbon dioxide, may be good for some. For most people, however, the downsides of climate change are likely to far outweigh the benefits. Don’t let Fox News mislead you. As a prudent, conservative people, we should take serious steps to mitigate our impact.

Dr. Pete Wyckoff is Associate Professor of Biology at the University of Minnesota, Morris.

The buggy comment registration bites us again. There was an interesting discussion between a reader, Don Baccus, and Pete Wyckoff about a small misconception in his editorial. Since they couldn’t post it in a comment, I’m putting it here.

I tried to post this to PZ Myers’ blog (about tree ring proxy temp reconstructs)

But it requires registration, and when I registered, the promised confirmation e-mail never arrived (not even in my junk folder).

You’ve got the “divergence problem” backwards, I think – the problem is there’s a *decline* in the tree ring widths in recent decades, while your description of CO2 effects, if I understand correctly, would lead to an *increase*.

That’s the “hide the decline” comment, “decline” in this case refers to the “divergence problem” (divergence from the instrumental temperature record).

Several leading candidates for the cause of this problem are anthropogenic, though, primarily air pollution. And apparently none of the researchers looking into this believe that the divergence problem indicates any problem with the reconstructions deeper into the past, except possibly during periods as warm as today (but other proxies tell researchers that on a global scale, at least, there hasn’t been such a period for 1,000+ years), and where the timeframes overlap, the tree ring reconstructions map other proxy reconstructions quite nicely. The leading natural, non-anthropogenic candidate appears to be drought, i.e. at a certain temperature threshold drought dominates for those locations that show the problem (BTW not all of the tree ring reconstructions show these problems).

Here’s a recent (2007) survey paper on the divergence problem:

http://www.ldeo.columbia.edu/~liepert/pdf/DArrigo_etal.pdf

Anyway, though you might want to dig a little deeper into this …

—-
Don Baccus
http://donb.photo.net
http://birdnotes.net
http://openacs.org

This is from Pete Wyckoff:

Hey Paul (and Don),

Thanks for picking up my editorial–one of your alert readers has pointed me to an area where my thinking was perhaps muddied by my temperate forest bias. In a 2008 paper in Global and Planetary Change (vol 60, pp 289-305), D’Arrigo et al. discuss possible causes for the “divergence problem” as it applies to very high latitude tree ring records. Not only have some of those records become merely unclear (which could well be carbon dioxide-related), but the particular ring records that caused Mann et al. problems did actually show a decline in growth despite increased temperatures. (To make things even more complicated, I believe the problematic records were based on ring density, not ring width, which is the metric I use in my work). As many of your commenters have correctly pointed out, carbon dioxide fertilization and carbon dioxide-induced drought tolerance can explain the loss of a climate signal, or an artificially enhanced growth signal, but are not likely to jive with a failure to grow.

In reading D’Arrigo et al., my lay person summary for what is going on is this: the Artic is rapidly warming. The trees that we might naively expect to rejoice at this development are instead showing signs of stress. The possible reason for this (of the many presented) that I find most convincing is that the warming is changing the regional hydrology to the point where trees are drought stressed so severely that they just can’t take advantage of the warmth–despite the rise in carbon dioxide!

How did I become confused in the first place? Well, for one, I’m a scientist and I am human, and when I saw a hot topic where my own work seemed relevant (which it is), I immediately jumped to a conclusion that inflated the connection to my own work. I was also led astray by a discussion of the “hide the decline” controversy (which I found disappointingly terse) on RealClimate that linked Briffa et al’s 1998 paper “Trees tell of past climates: but are they speaking less clearly today? “

Is there a way to get this posted? I’m pretty ignorant about how the whole blog-discussion thing is supposed to work.

Back to grading. I keep resolving to give shorter finals, but I never actually follow through.

Cheers,

Pete
PS. Don Baccus seems to be both a computer guy and a excellent nature photographer. Check out his on-line galleries.

Don Baccus replies:

Thanks for the response.

The D’Arrigo 2008 Global and Planetary Change paper is probably the same paper (perhaps modified to meet reviewer critiques) that I linked to as being “in press” in 2007?

Or is it a later paper with more info? If so, I’d appreciate a URL if it’s not behind a firewall (being a humble software engineer and, as you note, photographer, I’m not plugged into the climate science/dendro/biology infrastructure and have no academic access).

It’s interesting stuff … not interesting in the way that the rabid anti-science fuckhead (pardon me!) reality-denying luddite denialsphere types are saying, though. It’s interesting in the true scientific sense … what’s going on today that causes this subset of chronologies to diverge?

Here …

” (To make things even more complicated, I believe the problematic records were based on ring density, not ring width, which is the metric I use in my work)”

Yes, “maximum latewood density” apparently jargoned into “MXD” … high altitude/high latitude trees in the right circumstances apparently (you tell me, you’re the expert!) show most growth in a few short weeks in summer, and therefore are temperature-sensitive (more weeks of sufficiently warm weather means more growth). Makes sense to me, but my professional biology experience is limited to being a field tech doing raptor migration work. All I know about plants is that sometimes they grow, sometimes they don’t, and in field camp sometimes I burn them to keep warm :) Anyway, the claim is that this is a better metric for temperature sensitivity than simple tree ring width, and I believe it, from what I’ve read. In the sense that I trust experts, just as I’d hope you’d give me similar respect if you asked me about a computer science question.

“The possible reason for this (of the many presented) that I find most convincing is that the warming is changing the regional hydrology to the point where trees are drought stressed so severely that they just can’t take advantage of the warmth–despite the rise in carbon dioxide!”

This is the leading non-anthropogenic candidate …

I think the major problem researchers are having with this, though, is that the divergence problem is sort of randomly distributed with no immediately obvious correlation with available precip info. Then again, by definition, “high latitude” means “remote” and “no nearby (usually) met stations” so microclimate etc problems are well, problems. But I do think this is a very strong candidate (and if D`Arrigo 2008 states this more strongly, beyond her 2007 draft, perhaps even stronger, I’d like to read the latest paper rather than just the 2007 draft).

But all that holds true for possible anthropogenic causes. There’s a lack of localized data, I think that’s a big problem here in terms of pinning down the cause of the divergence problem.

But none of this seriously calls into question reconstructions that match available proxy and instrument data for like 90% or so of the period in which the data overlaps. Even the recent divergence problem in areas that have long term data available overlaps with thermometers for about 2/3 of the historical record (one reason why they think that some anthropogenic cause might be there, or a temperature threshold causing drought cause (which would make the denialist claims of a “warm as today” MWP even weaker than they are now, because you don’t see divergence back then)).

And of course, there are chronologies that don’t show the divergence problem at all, something the denialists are strangely quiet about …

Anyway the rational response to the divergence problem is to research it. Not to use it as a basis for claiming that all of science that might bear on climatology is a fraud :) I know I’ll be interested in what researchers find out about this over the next five to ten years …

Thank you very much for your response, and for taking the time to do some reading based on my e-mail, and for taking the time to respond.

And, PZ, thank you for being such a bulldog for what’s right and against what’s wrong.

PS. Don Baccus seems to be both a computer guy and a excellent nature photographer. Check out his on-line galleries.

And thanks for that, too :)

—-
Don Baccus
http://donb.photo.net
http://birdnotes.net
http://openacs.org

And one more from Baccus:

On Dec 17, 2009, at 8:31 PM, Peter Wyckoff wrote:

How did I become confused in the first place? Well, for one, I’m a scientist and I am human, and when I saw a hot topic where my own work seemed relevant (which it is), I immediately jumped to a conclusion that inflated the connection to my own work. I was also led astray by a discussion of the “hide the decline” controversy (which I found disappointingly terse) on RealClimate that linked Briffa et al’s 1998 paper “Trees tell of past climates: but are they speaking less clearly today? “

Regarding the Real Climate stuff … the terseness comes, partly, I believe, from the fact that climate science is so under the microscope that the anti-science/pseudoscience and the rational people share vocabulary and background to such an extent that such terseness is perfectly clear to those of us who are fixated on it.

Not much different than the biology vs. genesis (in all its permutations) debate. We all can talk in code, now, and if you don’t know it, it can seem terse.

Oh, and I missed that Real Climate link to the 2008 paper, I’d found the D’Arrigo 2007 in press work via google …

BTW I hope you don’t think that I don’t think you or any working scientist isn’t human, and are incapable of making mistakes, or having human feelings, and all that :) Or that your response in any way reflects on your expertise in the stuff you work on.

Is there a way to get this posted? I’m pretty ignorant about how the whole blog-discussion thing is supposed to work.

The way it’s supposed to work is that working scientists are supposed to be shouted down and humiliated by torch-burning, castle-storming Rush Limbaugh-worshipping “true Americans”. Filmed in black-and-white like the original Frankenstein movie, appropriate for the anti-progress mindset of these people.

And if scientists don’t crawl away and hide their research … death threats, attempts to get them fired, censured, etc.

(I’m not kidding, one climate scientist in Texas was given a police bodyguard before giving a talk in the last couple of months because of death threats, and scientists at CRU and Ben Santer at LLNL have gotten death threats, Ben Santer as far back as 1996, and they’re not the only ones). At this week’s AGU, a scientist at Penn State said an alumni tried to get him fired for saying “there’s no peer reviewed papers that overturn mainstream climate science” (paraphrase). James Hansen reports he and his co-workers are now spending much of their time working on FOIA requests that ask for all their correspondence to be released into the public domain.

Fear for science, dudes. The far right, especially here in the US, wants to bury science in the name of both extreme biblical literalism and libertarianism.

Anyway, thanks again, Peter, for your response.

—-
Don Baccus
http://donb.photo.net
http://birdnotes.net
http://openacs.org

Isaac Asimov and the fuzzy nature of knowledge

It’s an odd thing that when people list great science popularizers of the past, names like Sagan and Feynman always pop up, but most people seem to have forgotten Isaac Asimov, who wrote some fabulous essays on understanding science. Here’s one example, in which he addresses a claim we hear all the time, that the errors of the past mean our knowledge now is on very shaky ground. He’s answering a complaint from an English Lit student who chastised Asimov for thinking he knew anything at all.

The young specialist in English Lit, having quoted me, went on to lecture me severely on the fact that in every century people have thought they understood the universe at last, and in every century they were proved to be wrong. It follows that the one thing we can say about our modern “knowledge” is that it is wrong. The young man then quoted with approval what Socrates had said on learning that the Delphic oracle had proclaimed him the wisest man in Greece. “If I am the wisest man,” said Socrates, “it is because I alone know that I know nothing.” the implication was that I was very foolish because I was under the impression I knew a great deal.

My answer to him was, “John, when people thought the earth was flat, they were wrong. When people thought the earth was spherical, they were wrong. But if you think that thinking the earth is spherical is just as wrong as thinking the earth is flat, then your view is wronger than both of them put together.”

The basic trouble, you see, is that people think that “right” and “wrong” are absolute; that everything that isn’t perfectly and completely right is totally and equally wrong.

However, I don’t think that’s so. It seems to me that right and wrong are fuzzy concepts, and I will devote this essay to an explanation of why I think so.

Go read the rest, it’s worth the time.

God is a sockpuppet

So true and so hilarious: a study has found that god speaks with a remarkably egocentric voice. In tests that asked people what god’s opinion of various matters was, the unsurprising discovery was that it was the same as the individual’s opinion — and of course every person’s opinion was different. You’d expect some consistency if they were all hearing god’s word, you would think!

It fits with the typical vision of the sockpuppeteer, too: the loser whose opinions are indefensible, so he invents an army of aliases to agree with him. And what more powerful sockpuppet could there be than to have your arm up a god’s butt?

Get your geek on for Thursday

I’m going to be opening my mouth again on Thursday in Minneapolis — I’ll be giving a talk in MCB 3-120 on the Minneapolis campus at 7:30 on Thursday, 3 December. This will be open to the public, and it will also be an all-science talk, geared for a general audience. I’d say they were going to check your nerd credentials at the door, but just showing up means you’re already fully qualified.

The subject of the talk is my 3 big interests: a) evolution, or how we got here over multiple generations, b) development, or how we got here in a single generation, and c) the nervous system, the most complicated tissue we have. I intend to give a rough outline of how nervous tissue works, how it is assembled into a working brain, and how something so elaborate could have evolved. All in one hour. Wheee!

Afterwards, we’ll be joining the CASH gang for refreshments, somewhere. They haven’t told me yet where, but I know they’re fond of pizza.

IGERT2009: Sunday morning session

My little laptop is functional again, so at least I’ll be able to blog these Sunday morning IGERT sessions in real-time. I still have to transcribe my notes from yesterday; I’ll plan on getting that done on the plane this afternoon.

Kristi Montooth: Mitochondrial-nuclear epistasis for metabolic fitness in flies

How do physiological systems evolve to maintain metabolic fitness? This is a process that involves interactions between two genomes, the nuclear and mitochondrial. Energy metabolism is important and is the target of mutation, but the same players are found all across the tree of life, suggesting that there is also strong selective pressure to maintain a common system.

Montooth is looking at inducible gene expression: is there an energetic cost to switch genes off and on? She’s using respirometers that can measure the metabolic rate of single flies or larva. Flies are subjected to heat shock, which switches on HSP70. Flies normally have 6 copies of HSP70; they have mutants with 12, and they show a much greater rise in metabolic rate in response to heat shock.

Mitochondria are the source of the energy for this response. Mitochondria also have a high mutation rate and show strong linkage (no sexual recombination to cover for errors that arise). She’s arguing for selection for compensatory evolution in the nuclear genome, and the accumulation of intergenomic epistasis. To dissect the effects of coevolution of mitochondria and nuclear genomes, she transplanted mitochondria from different species into Drosophila melanogaster. These have between 18 and 100 amino acid substitutions from the Dmel sequence.

She plots mitochondrial genome in order of increasing divergence against measured fitness (she used a competition assay that she did not describe in detail). There is no correlation seen at all. Also, high fitness X/mtDNA genotypes in one sex can be low fitness genotypes in the other sex. Interactions between the X and mtDNA can maintain variation in both genomes. All of the fitness effects, with one exception, are subtle.

Some of the transgenomic effects have very strong effects on female fecundity, developmental rates, and locomotion. But adult metabolic rate shows no difference! The idea is that there are lots of homeostatic mechanisms that maintain metabolism very tightly, which then have secondary effects.

Johanna Schmitt: Adaptive evolution of Arabidopsis flowering pathways in different climates

Schmitt does ecological development, looking at the timing of plant development in different environments. How does phenology respond and adapt to climate variation? We expect evolution to adapt to variation in seasonal timing. The signaling pathways in Arabidopsis are well known; they respond to hormones, photoperiod, and ambient temperature by way of a fairly complicated set of pathways she showed us in a slide…sorry, no way I can reproduce it here!

Across its range, it shows a great deal of life history variation; one pattern in the Mediterranean, another in colder northern climes, and yet another in Northern Scandinavia, varying in how much time they spend in vegetative rosettes vs. bolting and flower production. Questions: are there are genetic variants associated with different life history patterns, can they identify the genes, and can they perturb them?

The experiments involved massive plantings in different sites in Europe with different climates, with different mutants. Is natural variation in candidate genes involved in variation in flowering time? They studied FRIGIDA, a gene that effects the vernalization pathway. When you lose FRIGIDA, you should see much more rapid flowering. Loss of function in this gene has evolved multiple times in northwestern Europe. The effect depends on the timing of planting and climate.

The effect of the mutant varies across geography, and they have a photothermal model of flowering time. The plants are tracking light and temperature, and the different mutants are counting up these inputs in slightly different ways. They can use this model to make predictions on the effects of FRIGIDA on flowering time with changes in germination timing, and then test these in the next year with plantings at different times and in their different geographical sites, and the model is working accurately.

They are also plugging in predicted future climate change from NOAA, and asking what we can expect to see 100 years from now; she showed maps of expected flowering times in 2100. They are also making predictions of the expected distributions of FRIGIDA alleles over time, and they hope to do the same for many other alleles in Arabidopsis.

Artyom Kopp: How the fly got its sexy legs – the origin and evolution of Drosophila sex combs

The sex comb is a male specific structure on the front legs which most Drosophila species lack — it’s a fairly recent innovation. How do you evolve a novel structure?

It’s limited to the melanogaster and obscura species groups, with quite a bit of diversity in different species, varying from 2-50 teeth, location, and arrangement. How do you go from sexually monomorphic state of a generically hairy leg to one with a specific bristle arrangement in males? The sex comb in males is homologous to a subset of bristles also found in females; in males, that patch of epidermis rotates 90° and the bristles enlarge. He showed a very pretty developmental series of this epithelium undergoing cell shape changes that move the bristles to a new location. Other species show similar morphological remodeling, but sometimes with some significant differences: D. kikkawai doesn’t do the rotation, but instead the bristle precursors arise in their final position. These modes do not cluster together phylogenetically, so these are examples of convergent evolution, generating similar structures with different mechanisms.

They are taking apart the genetics and regulatory inputs of sex comb development. Basically, it involves just about everything. It seems to arise by an interaction between Hox and sex determination genes. Spatial modulation of Sex combs reduced controls sex comb position. Scr in pupa; stages is only expressed in a limited domain in the leg, and ectopic expression of Scr produces multiple sex combs. Expression is also sexually dimorphic, with no upregulation of Scr in female legs. In D. ficusphila, which has enormous sex combs, Scr levels are elevated yet further to 7 times the levels found in D. willistoni.

The sex determination gene Double sex is also spatially patterned, and is refined and elevated to high levels in the area around the developing sex combs. Ectopic expression of Dsx induces ectopic sex combs.

How can a new developmental pathway evolve? In the ancestral condition, Scr is controlled by spatial cues to produce segmental patterns of bristles; in the sex-comb carrying species, Scr is coupled to Dsx. This explains the spatial pattern of gene expression, but it also needs to acquire new downstream targets to, for instance, regulate epidermal rotations.

Drosophila are old, and many of these species differences are millions of years old. They are now looking at more recently diverged species with differences in sex comb morphology, and are looking for correlations between Scr and species divergence.

And with that, I have to run for the airport shuttle. Good talks, and I unfortunately have to miss Rudy Raff’s wrap-up of the meeting.