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.

A creationist at the Chicago meeting

Last week, I described the lectures I attended at the Chicago 2009 Darwin meetings (Science Life also blogged the event). Two of the talks that were highlights of the meeting for me were the discussions of stickleback evolution by David Kingsley and oldfield mouse evolution by Hopi Hoekstra — seriously, if I were half my age right now, I’d be knocking on their doors, asking if they had room for a grad student or post-doc or bottle-washer. They are using modern techniques in genetics and molecular biology to look at variation in natural populations in the wild, and working out the precise genetic changes that led to the evolution of differences in development and morphology. They are doing stuff that, back when I actually was a graduate student, would have been regarded as technically impossible; you needed model systems in the laboratory to have the depth of molecular information required to track down the molecular basis of novel morphs, and you couldn’t possibly just grab some interesting but otherwise unknown species out on a beach or a pond and work out a map and localize genetic differences between individuals. They’re doing it now, though, and making it look easy.

Then there were all the other talks in population genetics and paleontology (and the talks on history and philosophy, which I almost entirely neglected)…this was a meeting that everywhere demonstrated major advances in our understanding of evolution. Every talk was about the successes of evolutionary theory and directions to take to overcome incomplete areas of understanding; this was a wonderfully positive and promising event that should have impressed all the attendees with the quality of the work that has been done and the excitement of the potential for future research. Like I said, there were a whole bunch of people here that I want to be when I grow up.

Well, normal people would feel that way. Paul Nelson, that creationist, was also there. Nelson is a weird guy; he’s always hanging around the edges of these scientific meetings, and you’d think that after all these years of lurking, he’d actually learn something, but no…the only skill he has mastered is the art of ignoring what he doesn’t like and incorporating fragments of sentences into his armor of ignorance. It’s very sad.

I talked with Nelson briefly at a reception at the meetings, and we both agreed on the quality of Kingsley’s work — but that’s about all. Nelson thought it supported ID better than neo-Darwinian evolutionary theory. His argument was that a) all anybody ever described was loss of features, and b) a large parent population was the source of all the allelic variation in the sub-populations studied, which is what ID predicts. He didn’t mention their favorite magic word of “front-loading”, but I could see what he was thinking.

How Nelson can hang about on the fringes of the evo-devo world and not notice that what was described by modern empirical research is exactly what the evo-devo theoreticians expected is a mystery — these were results that fit beautifully what science, not the wishful voodoo of intelligent design creationism, predicts.

Both Kingsley and Hoekstra are looking at recent species, subpopulations that separated from parent populations within the last ten thousand years, and have adapted relatively rapidly to new environmental conditions. The sticklebacks are fragments of marine species that were isolated in freshwater streams and lakes, while the beach mice are parts of a widespread population of oldfield mice that are adapting to gulf coast islands. They are also working with populations that can be bred back to the root stock, that retain the ability to do genetic crosses, so of course the variation is not on the magnitude of turning fins into limbs (we need large amounts of geological time to do that; it’s the kind of work Neil Shubin would do, and unfortunately, he can’t cross Tiktaalik with Acanthostega). Complaining that the variants the real scientists are looking at aren’t the kind that the creationists want is a particularly clueless kind of whine, since the scientists are intentionally focusing on the variants that are amenable to dissection by their techniques.

The other aspect of their work that confirms evo-devo expectations is that what they’re discovering is that the genetic mechanisms behind morphological variants are changes in regulatory DNA — that what’s happening is that regulatory genes like Pitx1 or Mc1r are being switched off or on. We anticipate that a lot of morphological novelty is going to be generated by switching genes off and on, and by recombination of patterns of gene expression. Nelson and Behe are reduced to carping on the sidelines that observed variants are just the product of getting large effects by trivially flipping switches, while all the real biologists are out there in the middle of the work happily announcing that we can get large-scale morphological effects by simply flipping switches, and hey, isn’t that cool, and doesn’t that tell us a lot about the origins of evolutionary novelties? It’s not just a to-may-to/to-mah-to difference in interpretation, this is a case of the creationists wilfully and ignorantly missing the whole point of an exciting line of research.

There’s also a fundamental failure of comprehension. Creationists see loss of a feature like pelvic spines, or a reduction in pigmentation, and declare that the evolutionary evidence is “all breaking things and losing things”. Wrong. What we have here is a complete lack of understanding of developmental genetics. What we typically find are changes in the pattern of expression of developmental genes, not wholesale losses. In the stickleback, Pitx1 is still there; what’s different is that the places in the embryo where it is turned on have changed, the map of the pattern of gene expression has shifted. You cannot describe that as simply a broken gene. Similarly, in the mouse, Hoekstra showed that the expression of genes that reduce pigmentation has expanded. We’ve seen the same thing in the blind cavefish; a creationist looks at it and says it’s just broken and has lost its eyes, but the scientists look closer and see that no, the fish have actually increased gene expression and expanded the domain of a midline gene.

Just wait for the detailed analysis of jaw morphology in cichlid fishes. These animals have radically different variants in feeding structures, which is thought to be the root of their adaptability and the radiation of different forms, and I guarantee you that the creationists will ignore the morphological novelties and focus on the fact that to achieve that, some genes will be downregulated (I also guarantee you that there will be such shifts in expression). It’s “all breaking things and losing things”, after all; just like baking a cake involves breaking eggs.

I don’t know how the creationists fit known variations in the coding sequences of genes (how do you translate a single-nucleotide polymorphism into their vision of all change being a matter of losses?) into their idea that all evolution is a matter of breaking DNA, or how they can claim all novelty requires a designer when people can track the progression of morphological shifts in the tetrapod transition, for instance, across tens of millions of years. It seems to be their desperate 21st century excuse in the face of the overwhelming progression of information from 21st century biological science.

Nelson ends his skewed summary of the meeting with the comment that “It’s a heck of a lot of fun to attend a conference like this, if you don’t mind being the butt of jokes.” I’m sure. I suppose Nelson could have even more fun if he put on a dunce cap and drooled a lot, because that’s basically his role at these meetings anyway — he’s the butt of jokes because he shows up and then happily demonstrates his ignorance about what’s going on. It’s not a role I’d enjoy, but the gang at the clown college called the Discovery Institute have a slightly different perspective, I suppose.

William Wimsatt—Why Development is Crucial to Cultural Evolution

Man, philosophers sure take a long time to get to the point.

OK, his outline: 1) development and differential entrenchment in evolution. 2) application of these principles to culture. 3) what new phenomena this theory can capture.

Plunges into “thick, thin, and medium viscosity theories of culture”. I have no idea what he’s talking about: I hope he’ll get into some specifics I can grapple with soon, because right now this is just a wall of words.

Any evolving system must meet Darwin’s principles: variation, which is heritable, which has consequences on fitness. Wimsatt suggests two additional principles: structures generated over time have a developmental history, and they have parts which have larger or more pervasive effects than others on that production. Wimsatt says that life cycles emerge from these principles, and illustrates it with some strange models.

I give up. I have no idea where this talk is going. I keep waiting for an empirical foundation to be dragged in from offstage, but it’s just not happening. He seems to be saying some interesting stuff (or stuff that should be interesting), but it all seems to be built on air.

I don’t think I could ever be a philosopher.

Hopi Hoekstra—The Causes of Evolutionary Change: What Darwin Did and Didn’t Know

Darwin didn’t know the basic mechanisms of evolutionary change. Mechanism of inheritance was a black box. Darwin’s last publication before his death was “on the dispersal of bivalves”. Why are freshwater bivalves so homogeneous in morphology? Describes a beetle with a conch attached to its leg, which provided a mechanism of dispersal. Turns out the specimen was sent to Darwin by Crick’s grandfather.

How is variation generated and maintained in natural populations? What genes matter? What will finding the genes tell us?

We find genes underlying phenotypic diversity by comparison of highly divergent taxa (flies vs. mice, for instance), or the study of variation within species. Latter gives us the opportunity to use genetics, also allows us to know something about the environmental context that drives the differences.

Looks for phenotypic differences in the wild that contribute to fitness, then works out the genetics and development to see how it works. Hoekstra looks at color, the genetics of mammalian pigmentation in Peromyscus. These mice show lots of variation in color. The oldfield mouse of the American south lives in abandoned fields and on beaches. Beach sand is white, with low levels of vegetation, which means they are subject to high levels of predation. They wanted to document the selective advantage of light pigmentation on the beach environment, so made model mice out of clay with different colors,. and measured predation on the models. Color matters, and dark models were attacked preferentially on light sand, light models attacked in dark environments. 50% more likely to survive if your color matches your background.

Made crosses of dark and light genes and used QTL analysis to search for candidate genes. Found 3 genes correlated with the color patterns seen in Peromyscus, Mc1r, Agouti, and Corin. Mc1r is a g-coupled receptor with many mutations scattered throughout the gene. One difference is found between light and dark mice: changing one amino acid reduces the activity of the gene product.

Mc1r is the receptor; agouti is a repressor of mc1r; and Corin is an upstream regulator of agouti.

Looked at populations in the wild. Do populations on the gulf coast have the same mutation as atlantic coast mice? No — atlantic mice do not have the same mutation im mc1r, and no significant mutations were found in the atlantic mc1r.

Going even further afield, mc1r was sequenced in mammoths, and the same mutation found in light mice was found in mammoths; were mammoths polymorphic in coat color?

What do these genes tell us? 1) how many and and what are the effect sizes of genes that contribute to adaptive phenotypes? A few genes can have a large affect. 2) Do adaptive alleles tend to be dominant or recessive? Adaptive alleles are rarely completely recessive. 3) What is the relative role of epistasis versus additivity? Epistasis is very important. 4) Are the same genes responsible for convergent phenotypes? sometimes, but not the case within beach mice. 5)Are adaptive mutations in protein-coding or cis-regulatory regions? Both.

Michael Ruse—Is Darwinism past its ‘sell by’ date? The challenge of evo-devo

How can I resist an opportunity to see Ruse gibbering on the stage? I’m curious to see whether he annoys or enlightens. It could go either way.

He’s not going to talk about evo-devo! OK, I’m already annoyed.

Criticizes the infamous New Scientist cover, “Darwin Was Wrong”; received email from Paul Nelson (boo) claiming the edifice of darwinism is crumbling; Rudy Raff has written that evolution requires development to remain relevant. Are today’s evolutionists genuinely Darwinian or not?

Plans to pick on something that was self-consciously in Darwin’s thinking. Darwin became an evolutionist in 1837 while analyzing the specimens he had collected on his voyage; he became a Darwinian in 1838 when he realized the mechanism of adaptive change, natural selection.

William Whewell was a major influence. Whewell tried to define good science: identifying a true cause, which is a hypothesis that explains the evidence. Darwin doesn’t see evolution at work, but the evidence is marshalled to point to the hypothesis. He’s not doing the original research, but picking it up and putting it together in a new and powerful way. Fossils, biogeography, homology, embryology, etc. all were assembled to support his theory.

Did Darwin trigger a paradigm shift? Huxley didn’t appreciate natural selection at all. It took the rediscovery of Mendel, popgen, etc. to bring about a major appreciation of the theory. Further revision with the synthetic theory that incorporated molecular biology.

Positively reviewed Dawkins’ latest book, and Dawkins is contemptuous of eyewitness testimony, but says the theory demands respect because of the volume of evidence, which is clearly in the spirit of Darwin and Whewell.

EO Wilson’s work on ants show the amazing specialization of castes in particular distributions. This is material Darwin never considered, but Wilson is using the tools of evolutionary biology to explain his hypotheses.

Pre-Cambrian was terra-incognito to Darwin; he had many ad hoc hypotheses to explain why we don’t have specimens from that era. Modern explanations do a better job of fitting the pre-Cambrian into a Darwinian framework.

We know much more about human evolution, extinction, geographical distributions (plate tectonics) than Darwin did, but these are still thoroughly explained by Darwin’s ideas.

Hox genes show deep homology between flies and humans, also interpreted in a Darwinian context.

Draws an analogy with the Volkswagen, which was completely different between the 40s and modern day, with no parts that are identical, and yet it is obviously linked. We will still be celebrating Darwin 100 years from now because we will still be using his ideas.

OK, not bad, not too annoying. Needed more evo-devo. Philosophers sure do talk a lot; this talk was definitely not as information-dense as the biology sessions.

Neil Shubin—“Major Transitions” in Evolution: Fossils, Genes, and Embryos

Shubin had a tough act to follow, coming after Kingsley’s great talk. I’m sure it will be good, though — last night I got a tour of his lab, saw the original Tiktaalik specimens and some new ones, and some of his work in progress (which I won’t tell you about until it’s published), so I’m confident I’m going to have a happy hour.

Darwin pulled together diverse lines of evidence to document his ideas. The different lines all reinforce each other making the argument even stronger, and what we’re seeing now is new syntheses, which is the theme of this talk: how do we use different lines of evidence to make a case that is more the sum of its parts.

The questions is the origin of limbs, fins to legs. Fins and legs look very different, with fins having rays and many bones, while legs have few bones in a fixed pattern. Intermediate taxa show us the changes, with transitions with bony core of the limb pattern and fish-like rays. He uses geology and extant fossils to make predictions about where to find intermediates, and paleontology also informs his understanding of developmental processes that build the limb.

Began his work in Pennsylvania, which was like the Amazon delta 360 million years ago. They followed the PA dept. of transportation around looking at road cuts that exposed the rocks of that age. They found many fossils, but one that changed his thinking was a fin of sauripterus, with fin rays and a core of tetrapod-like limbs. Definitely fishy, but contained precursors to the pattern.

They searched in Ellesmere Island for Devonian age rocks and fossils that would reveal the history of the limb. The logistics were very difficult, since the area is inaccessible. First started working in 1999, in rocks that were from marine sources and didn’t yield much. Moved east to freshwater sources. Found a layer of rock that was rich in bone, and found a snout of a flat-headed fish poking out. Eventually exposed about 20 specimens of this animal. Took months to fully expose the details of the specimen.

He showed off a cast of Tiktaalik — physical objects are really good at capturing people’s imagination.

It took a year and a half to prepare out the fins; the bones show articular surfaces, so you can actually see how the structure bent in life. What does this tell us about extant fins?

A tetrapod limb has 3 components: 1 bone, then 2 bones, then multiple bones in wrist and fingers. The limb forms in phases, with an early phase of hox expression that sets up the proximal bone, then phase II in which hox genes switch on in a patterned way to form digits. Are there elements of phase 2 in fish fins?

Looked in Polyodon, and embryos do have a distal phase of hox expression, not identical to tetrapod pattern, but definitely a phase 2.

What is a limb and how did it develop? The AER sets up the proximo-distal axis, ZPA sets up anteriorposterior axis. Cutting off the AER at different stages produces progressive deletions of portions of the limb. ZPA is a source of Sonic Hedgehog and sets up a gradient of positional information.

Does the common ancestor of all fish have these same two-axis signals? Chondrichthyans do, with patterns that can be manipulated in the same way as we do in chickens. The appendage patterning system is general to all vertebrate appendages.

How do fins differ from other outgrowths? Branchial arches have the same patterning, with an AER and ZPA. Seems to be a universal way for vertebrates to set up the patterning of outgrowths. Gill, fin, and limb have similar toolkits of patterning genes.

The patterning mechanisms may have originated in a general outgrowth and been coopted for limbs and gills. Shubin proposes to do targeted collecting of Ordovician vertebrates, expecting to find novel non-limb outgrowths that may be precursors to the patterning mechanism. Paleontology guided by developmental biology!

David Kingsley—Fishing for the Secrets of Vertebrate Evolution

This talk should put me back in my comfort zone—developmental biology, evolution, and fish, with the stickleback story, one of the really cool model systems that have emerged to study those subjects.

What is the molecular basis of evolutionary change in nature? How many genetic changes are required to produce new traits? Which genes are used? What types of mutations? Few or many changes required?

The dream experiment would be to cross a whale and a bat and figure out what their genetic differences are. That’s impossible, so they searched for other organisms with a suite of differences that were crossable…and they picked the 3-spined stickleback.

Sticklebacks are migratory between salt and freshwater, and post-glaciation, they colonized many freshwater lakes and streams. The marine phenotype is ancestral, and freshwater species have many differences…but because these differences only evolved in the past 10-20,000 years, and they are crossable by artificial insemination.

Fish are small, easy to collect, and have segregating genetic traits. They have disadvantages: no sequences, no clone libraries, no genetic markers, no linkage maps, no transgenic mehtods when first worked out. Now they have dense genetic and physical maps, a complete genome sequence, whole genome transcriptome arrays, genome wide SNP studies, and high throughput transgenics. Zoom.

Specific questions: hindlimb reduction occurs in many vertebrates. Marine sticklebacks have substantial pelvis, pelvic spines, and fins. Some of the freshwater populations have lost the hindfins in cases where predation is low, calcium is low, and there are many insect predators.

Crossing marine and freshwater with pelvic reductions identified single chromosomal region that explains 65% of the variance. They also have candidate genes: Gli3, Fgf10, Shh, Fgf8, Fgf4…most interested in ones expressed only in hindlimb: Pitx1, which maps directly to chromosome involved in reductions.

The protein coding region of Pitx1 is identical, but there is a tissue-specific loss of expression in the developing pelvic region. This is a gene of large effect.

Knocking out Pitx1 in mice yields reduced hindlimbs and death before birth. Regulatory changes are more focused and specific; cis-acting regulatory changes FTW!

Still need info. What base pairs have changed? Single or multi-step mutations? Same or different events in different populations? Are there hotspots?

Doing fine mapping of the defect: there are some populations that are dimorphic, in which the mutation is not yet fixed. They’ve identified a 20kb interval upstream of Pitx1 that is correlated with the differences. This sequence has been tied to a reporter gene, and it does contain a pelvic enhancer.

Can they reverse the change? Couple the 20kb sequence with a Pitx1 gene, put that in a pelvic-reduced fish, and presto, it restores a full and beautiful pelvis and pelvic spine. They think they have the right region.

Looking at different pelvic-reduced populations suggest that this pelvic control region is the target of many independent mutations. Is the Pitx1 gene predisposed to mutation? Sequence is full of repeats, might be comparable to a fragile site. This is a flexible region of DNA. Four of top ten flexibility scores in the whole stickleback genome are right in that 20kb region. The upstream coding region also exhibits other signatures of selection.

Another trait: armor plates. Marine forms are heavily armored, many freshwater species have reduced armor. Similar crosses have identified a region on one chromosome that accounts for much of the variation. Similar crosses done for skin color.

Pelvice, armor, and pigmentation mutations are all in regulatory genes. Mouse and human mutations in these same genes cause all sorts of severely deleterious effects (again, likely to be regulatory changes, not changes in the genes themselves). They are not knockout mutations in the fish, but only regulatory changes.

Same genes are involved in independent mutations in stickleback populations — how far might this similarity extend? The genes involved in stickleback pigmentation (kitlg) are also involved in human pigmentation variants. Variations in regulatory regions of kitlg account for 20% of the pigment variation in human populations, and these regions also show signs of selection. Currently injecting constructs with fish regulatory genes into mouse embryos and getting changes in pigmentation.

They’ve mapped many other traits to QTLs in the fish genome, but only 3 have been dug into deeply enough — lots of work left to do!

Interestingly, marine fish carry a haplotype for the variant alleles used in armor plating and pigmentation at low levels (0.5%-1.0%), and these are subject to selective sweeps in new freshwater populations that drive them to fixation. So we see the same alleles emerging with high frequency in different populations.

Fabulous stuff. I’m struggling to restrain myself from doing a Homer-like gurgle. Mmmm, sticklebacks.

David Jablonski—Paleontology and Evolutionary Biology: The Revitalized Parnership

Darwin had problems with the fossil record that he explained as a result of imperfections. Modern paleo has corrected some of that with the discovery of many intermediates. Jablonski is going to talk about the fossil record as a laboratory for testing evolutionary hypotheses. Marine bivalves are model systems with both modern forms and good fossil preservation for developing analysis techniques.

The fossil record gives access to raw rates of development, unique events, and long intervals, spatial dynamics, and morphological transitions in form.

Extinction in the fossil record is a problem. Huge variation in extinction intensity over time; there is also differential extinction of mollusc clades. There is no contant rate of extinction over time and across phylogenies.

Compared bivalve living clades with total clades over time.

Tropics are a cradle of new taxa that trickle up into the higher latitutdes; lineages preferentially arise in the tropics. Tropical origins seen despite poor fossil record in tropics, and occurs in spite of increasing harshness of higher latitudes over the same period.

Evolution of form: there is a pattern seen in fossils, (type 1) a rapid increase in morphological disparity early leading to taxonomic diversity, or (type 2) disparity and diversity rise together, or (type 3) morphological disparity is low, but diversity rises rapidly.

Echinoderms fit type 1; Aporrhaidae follow type 2 model; Trilobites are type 3, where stable body plan is accompanied by huge species diversity.He catalogs many lineages and characterizes which type they fall into. I’m a bit lost as to what point he’s trying to make here. OK, so there are different patterns of disparity and diversity in different lineages, but why is this interesting? I seem to be lacking some important background to follow this talk.

We get a question: Ecological opportunity is a key factor in diversity. Is it enough to generate the type 1 pattern of diversification? Alas, I don’t seem to get an answer.

For understanding long term patterns of change, we need both evolution and paleontology. Extinction varies temporally and among clades. Clades are spatioally dynamic and geographic histories are often surprising, and there are multiple pathways to prolific diversification.

This talk actually generated a fair number of questions, so I confess that I’m missing something here. It looks like I’m going to have to dig into a few Jablonski papers. Either that or I need more sleep/coffee.