Don’t faint. I met some people at this meeting.
What did you think, I’d strip half-naked, paint myself blue, and start swinging a broadsword?
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.
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.
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.
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!
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.
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.
Kimberly Daniels of the Christian Broadcasting Network has a warning for trick-or-treaters.
“[M]ost of the candy sold during this season has been dedicated and prayed over by witches,” Daniels wrote. “I do not buy candy during the Halloween season. Curses are sent through the tricks and treats of the innocent whether they get it by going door to door or by purchasing it from the local grocery store. The demons cannot tell the difference.”
I think Kimberly is just one of those obnoxious cheapskates who wants an excuse to hand out bible tracts on Halloween. Although, if I were a witch, I’d totally want a full-time job in a candy factory.