The molecular foundation of the phylotypic stage

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When last we left this subject, I had pointed out that the phenomenon of embryonic similarity within a phylum was real, and that the creationists were in a state of dishonest denial, arguing with archaic interpretations while trying to pretend the observations were false. I also explained that constraints on morphology during development were complex, and that it was going to take something like a thorough comparative analysis of large sets of gene expression data in order to drill down into the mechanisms behind the phylotypic stage.

Guess what? The comparative analysis of large sets of gene expression data is happening. And the creationists are wrong, again.

Again, briefly, here’s the phenomenon we’re trying to explain. On the left in the diagram below is the ‘developmental hourglass’: if you compare eggs from various species, and adults from various species, you find a diversity of forms. However, at one period in early development called the phylytypic stage (or pharyngula stage specifically in vertebrates), there is a period of greater similarity. Something is conserved in animals, and it’s not clear what; it’s not a single gene or anything as concrete as a sequence, but is instead a pattern of interactions between developmentally significant genes.

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The diagram on the right is an explanation for the observations on the left. What’s going on in development is an increase in complexity over time, shown by the gray line, but the level of global interactions does not increase so simply. What this means is that in development, modular structures are set up that can develop autonomously using only local information; think of an arm, for instance, that is initiated as a limb bud and then gradually differentiates into the bones and muscle and connective tissue of the limb without further central guidance. The developing arm does not need to consult with the toes or get information from the brain in order to grow properly. However, at some point, the limb bud has to be localized somewhere specific in relation to the toes and brain; it does require some sort of global positioning system to place it in the proper position on the embryo. What we want to know is what is the GPS signal for an embryo: what it looks like is that that set of signals is generated at the phylotypic stage, and that’s why this particular stage is relatively well-conserved.

One important fact about the diagram above: the graph on the right is entirely speculative and is only presented to illustrate the concept. It’s a bit fake, too—the real data would have to involve multiple genes and won’t be reducible to a single axis over time in quite this same way.

Two recent papers in Nature have examined the real molecular information behind the phylotypic stage, and they’ve confirmed the molecular basis of the conservation. Of course, by “recent”, I mean a few weeks ago…and there have already been several excellent reviews of the work. Matthew Cobb has a nice, clean summary of both, if you just want to get straight to the answer. Steve Matheson has a three part series thoroughly explaining the research, so if you want all the details, go there.

In the first paper by Kalinka and others, the authors focused on 6 species of Drosophila that were separated by as much as 40 million years of evolution, and examined quantitative gene expression data for over 3000 genes measured at 2 hour intervals. The end result of all that work is a large pile of numbers for each species and each gene that shows how expression varies over time.

Now the interesting part is that those species were compared, and a measure was made of how much the expression varied: that is, if gene X in Drosophila melanogaster had the same expression profile as the homologous gene X in D. simulans, then divergence was low; if gene X was expressed at different times to different degrees in the two species, then divergence was high. In addition, the degree of conservation of the gene sequences between the species were also estimated.

The prediction was that there ought to be a reduction of divergence during the phylotypic period. That is, the expression of genes in these six species should differ the least in developmental genes that were active during that period. In addition, these same genes should show a greater degree of evolutionary constraint.

Guess what? That’s exactly what they do see.

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Temporal expression divergence is minimized during the phylotypic period. a, Temporal divergence of gene expression at individual time points during embryogenesis. The curve is a second-order polynomial that fits best to the divergence data. Embryo images are three-dimensional renderings of time-lapse embryonic development of D. melanogaster using Selective Plane Illumination Microscopy (SPIM).

That trough in the graph represents a period of reduced gene expression variance between the species, and it corresponds to that phylotypic period. This is an independent confirmation of the morphological evidence: the similarities are real and they are an aspect of a conserved developmental program.

By the way, this pattern only emerges in developmental genes. They also examined genes involved in the immune system and metabolism, for instance, and they show no such correlation. This isn’t just a quirk of some functional constraint on general gene expression at one stage of development, but realy is something special about a developmental and evolutionary constraint.

The second paper by Domazet-Loso and Tautz takes a completely different approach. They examine the array of genes expressed at different times in embryonic development of the zebrafish, and then use a comparative analysis of the sequences of those genes against the sequences of genes from the genomic databases to assign a phylogenetic age to them. They call this phylostratigraphy. Each gene can be dated to the time of its origin, and then we can ask when phylogenetically old genes tend to be expressed during development.

The prediction here is that there would be a core of ancient, conserved genes that are important in establishing the body plan, and that they would be expressed during the phylotypic stage. The divergence at earlier and later stages would be a consequence of more novel genes.

Can you guess what they saw? Yeah, this is getting predictable. The observed pattern fits the prediction.

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(Click for larger image)

Transcriptome age profiles for the zebrafish ontogeny. a, Cumulative transcriptome age index (TAI) for the different developmental stages. The pink shaded area represents the presumptive phylotypic phase in vertebrates. The overall pattern is significant by repeated measures ANOVA (P = 2.4 3 10-15, after Greenhouse-Geisser correction P = 0.024). Grey shaded areas represent ± the standard error of TAI estimated by bootstrap analysis.

So what does this all tell us? That the phylotypic stage can be observed and measured quantitatively using several different techniques; that it represents a conserved pattern of development gene expression; and that the genes involved are phylogenetically old (as we’d expect if they are conserved.)

Domazet-Loso and Tautz propose two alternative explanations for the phenomenon, one of which I don’t find credible.

Adaptations are expected to occur primarily in response to altered ecological conditions. Juvenile and adults interact much more with ecological factors than embryos, which may even be a cause for fast postzygotic isolation. Similarly, the zygote may also react to environmental constraints, for example, via the amount of yolk provided in the egg. In contrast, mid-embryonic stages around the phylotypic phase are normally not in direct contact with the environment and are therefore less likely to be subject to ecological adaptations and evolutionary change. As already suggested by Darwin, this alone could explain the lowered morphological divergence of early ontogenetic stages compared to adults, which would obviate the need to invoke particular constraints. Alternatively, the constraint hypothesis would suggest that it is difficult for newly evolved genes to become recruited to strongly connected regulatory networks.

They propose two alternatives, that the phylotypic stage is privileged and therefore isn’t being shaped by selection, or that it is constrained by the presence of a complicated gene network, and therefore is limited in the amount of change that can be tolerated. The first explanation doesn’t make sense to me: if a system is freed from selection, then it ought to diverge more rapidly, not less. I’m also baffled by the suggestion that the mid-stage embryos are not in direct contact with the environment. Of course they are…it’s just possible that that mid-development environment is more stable and more conserved itself.

What we need to know more about is the specifics of the full regulatory network. A map of the full circuitry, rather than just aggregate measures of divergence, would be nice. I’m looking forward to it!

The creationists aren’t, though.

Domazet-Loso, T., & Tautz, D. (2010). A phylogenetically based transcriptome age index mirrors ontogenetic divergence patterns. Nature 468 (7325): 815-818. DOI: 10.1038/nature09632

Kalinka, A., Varga, K., Gerrard, D., Preibisch, S., Corcoran, D., Jarrells, J., Ohler, U., Bergman, C., Tomancak, P. (2010). Gene expression divergence recapitulates the developmental hourglass model. Nature 468 (7325): 811-814 DOI: 10.1038/nature09634

There’s plenty of time for evolution

This is a familiar creationist argument, stated in this case by a non-creationist:

Consider the replacement processes needed in order to change each of the resident genes at L loci in a more primitive genome into those of a more favorable, or advanced, gene. Suppose that at each such gene locus, the argument runs, the proportion of gene types (alleles) at that gene locus that are more favored than the primitive type is K−1. The probability that at all L loci a more favored gene type is obtained in one round of evolutionary “trials” is K−L, a vanishingly small amount. When trials are carried out sequentially over time, an exponentially large number of trials (of order KL) would be needed in order to carry out the complete transformation, and from this some have concluded that the evolution-by- mutation paradigm doesn’t work because of lack of time.

Basically, what creationists argue is that the evolution of new genes is linear and sequential — there is no history, no selection, it works entirely by random replacement of the whole shebang, hoping that in one dazzling bit of luck that the entire sequence clicks into the right sequence, and then it all works. If that were the way the process occurred, then they’d be right, and evolution would be absurdly improbable and would take an untenable length of time.

Another way to think of it is a bizarre version of the hangman guessing game, where one person thinks of a word, and the second person has to guess what it is. In the normal version of the game, the second person guesses letters one by one, and they’re placed in the appropriate spot. In the creationist version, you only get to guess a whole sequence of letters in each round, and you are only told if you are right or wrong, not which letters are in the correct position in the word. Not only does it become a really boring game, but it also becomes extremely unlikely that anyone can solve it in a reasonable amount of time.

Evolution does not work like that. It works in parallel, changing and testing each variant simultaneously in many individuals, and then selection for the most favorable subset of changes latches them in place, making the matching letters more likely to be fixed. Or, as the paper by Wilf and Ewens explains,

But a more appropriate model is the following. After guessing each of the letters, we are told which (if any) of the guessed letters are correct, and then those letters are retained. The second round of guessing is applied only for the incorrect letters that remain after this first round, and so forth. This procedure mimics the “in parallel” evolutionary process. The question concerns the statistics of the number of rounds needed to guess all of the letters of the word successfully.

That’s the question. If purely random changes would require a ridiculous length of time to match a target, proportional to KL, how long would it take if we actually use more reasonable, biologically relevant model? Wilf and Ewens state the model in mathematical terms and derive a theoretical answer, and you won’t be surprised that it’s significantly shorter; you might be impressed at how much shorter the operation would take.

Instead of a time proportional to KL, it will take a time proportional to K log L.

That’s very much shorter! To put some representative numbers on it, imagine a protein that is 300 amino acids long, made up of 20 possible amino acids, and I’m going to ask you to guess the sequence. Under the creationist model, you wouldn’t even want to play the game — it would take you on the order of 20300 trials to hit that one specific arrangement of amino acids. On the other hand, if you took a wild guess, writing down a random 300 amino acids, and I then told you which amino acids in which position were correct, you’d be able to progressively work out the exact sequence in only 20 log 300 trials, or around 50 guesses.

Notice that this is not a concrete estimate of the time it would take for something to evolve! It’s a grossly simplified version of the story: the example overstates the power of selection (amino acids won’t be locked in, but will only be less likely to change), and overstates the required accuracy of matching to a target (there would be more tolerance for variation), and the whole idea of meeting a specific target is not necessarily a good model. As a guide to short-circuiting the invalid assumptions of creationists, though, it’s handy to have a simple mathematical formula to remove that naive combinatorial model from the table.

Wilf HS, Ewens WJ (2010) There’s plenty of time for evolution. arXiv:1010.5178v1.

It’s not an arsenic-based life form

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Oh, great. I get to be the wet blanket.

There’s a lot of news going around right now about this NASA press release and paper in Science — before anyone had read the paper, there was some real crazy-eyed speculation out there. I was even sent some rather loony odds from a bookmaker that looked like this:

WHAT WILL NASA ANNOUNCE?

NASA HAS DISCOVERED A LIFE FORM ON MARS +200 33%
DISCOVERED EVIDENCE OF LIFE ON ONE OF SATURNS MOON +110 47%
ANNOUNCES A NEW MODEL FOR THE EXISTENCE OF LIFE -5000 98%
UNVEILS IMAGES OF A RECOVERED ALIEN SPACECRAFT +300 25%
CONFESSES THAT AREA 51 WAS USED FOR THE ALIEN STUDIES +500 16%

[The +/- Indicates the Return on the Wager. The percentage is the likelihood that response will occur. For Example: Betting on the candidate least likely to win would earn the most amount of money, should that happen.]

I think the bookie cleaned up on anyone goofy enough to make a bet on that.

Then the stories calmed down, and instead it was that they had discovered an earthly life form that used a radically different chemistry. I was dubious, even at that. And then I finally got the paper from Science, and I’m sorry to let you all down, but it’s none of the above. It’s an extremophile bacterium that can be coaxed into substiting arsenic for phosphorus in some of its basic biochemistry. It’s perfectly reasonable and interesting work in its own right, but it’s not radical, it’s not particularly surprising, and it’s especially not extraterrestrial. It’s the kind of thing that will get a sentence or three in biochemistry textbooks in the future.

Here’s the story. Life on earth uses six elements heavily in its chemistry: carbon, hydrogen, nitrogen, oxygen, phosphorus, and sulfur, also known as CHNOPS . There are other elements used in small amounts for specialized functions, too: zinc, for instance, is incorporated as a catalyst in certain enzymes. We also use significant quantities of some ions, specifically of sodium, potassium, calcium, and chloride, for osmotic balance and they also play a role in nervous system function and regulation; calcium, obviously, is heavily used in making the matrix of our skeletons. But for the most part, biochemistry is all about CHNOPS.

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Here’s part of the periodic table just to remind you of where these atoms are. You should recall from freshman chemistry that the table isn’t just an arbitrary arrangement — it actually is ordered by the properties of the elements, and, for instance, atoms in a column exhibit similar properties. There’s CHNOPS, and notice, just below phosphorous, there’s another atom, arsenic. You’d predict just from looking at the table that arsenic ought to have some chemical similarities to phosphorus, and you’d be right. Arsenic can substitute for phosphorus in many chemical reactions.

This is, in fact, one of the reasons arsenic is toxic. It’s similar, but not identical, to phosphorus, and can take its place in chemical reactions fundamental to life, for instance in the glycolytic pathway of basic metabolism. That it’s not identical, though, means that it actually gums up the process and brings it to a halt, blocking respiration and killing the cell by starving it of ATP.

Got it? Arsenic already participates in earthly chemistry, badly. It’s just off enough from phosphorus to bollix up the biology, so it’s generally bad for us to have it around.

What did the NASA paper do? Scientists started out the project with extremophile bacteria from Mono Lake in California. This is not a pleasant place for most living creatures: it’s an alkali lake with a pH of close to 10, and it also has high concentrations of arsenic (high being about 200 µM) dissolved in it. The bacteria living there were already adapted to tolerate the presence of arsenic, and the mechanism of that would be really interesting to know…but this work didn’t address that.

Next, what they did was culture the bacteria in the lab, and artificially jacked up the arsenic concentration, replacing all the phosphate (PO43-) with arsenate (AsO43-). The cells weren’t happy, growing at a much slower rate on arsenate than phosphate, but they still lived and they still grew. These are tough critters.

They also look different in these conditions. Below, the bacteria in (C) were grown on arsenate with no phosphate, while those in (D) grew on phosphate with no arsenate. The arsenate bacteria are bigger, but thin sections through them reveal that they are actually bloated with large vacuoles. What are they doing building up these fluid-filled spaces inside them? We don’t know, but it may be because some arsenate-containing molecules are less stable in water than their phosphate analogs, so they’re coping by generating internal partitions that exclude water.

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What they also found, and this is the cool part, is that they incorporated the arsenate into familiar compounds*. DNA has a backbone of sugars linked together by phosphate bonds, for instance; in these baceria, some of those phosphates were replaced by arsenate. Some amino acids, serine, tyrosine, and threonine, can be modified by phosphates, and arsenate was substituted there, too. What this tells us is that the machinery of these cells is tolerant enough of the differences between phosphate and arsenate that it can keep on working to some degree no matter which one is present.

So what does it all mean? It means that researchers have found that some earthly bacteria that live in literally poisonous environments are adapted to find the presence of arsenic dramatically less lethal, and that they can even incorporate arsenic into their routine, familiar chemistry.

It doesn’t say a lot about evolutionary history, I’m afraid. These are derived forms of bacteria that are adapting to artificially stringent environmental conditions, and they were found in a geologically young lake — so no, this is not the bacterium primeval. This lake also happens to be on Earth, not Saturn, although maybe being in California gives them extra weirdness points, so I don’t know that it can even say much about extraterrestrial life. It does say that life can survive in a surprisingly broad range of conditions, but we already knew that.

So it’s nice work, a small piece of the story of life, but not quite the earthshaking news the bookmakers were predicting.

*I’ve had it pointed out to me that they actually didn’t fully demonstrate even this. What they showed was that, in the bacteria raised in arsenates, the proportion of arsenic rose and the proportion of phosphorus fell, which suggests indirectly that there could have been a replacement of the phosphorus by arsenic.

Wolfe-Simon F,
Blum JS,
Kulp TR,
Gordon GW,
Hoeft SE,
Pett-Ridge J,
Stolz JF,
Webb SM,
Weber PK,
Davies PCW,
Anbar AD, Oremland RS (2010) A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus. Science DOI: 10.1126/science.1197258.

Lungs with taste, or lungs with a fortuitous receptor?

Researchers in Maryland have discovered an interesting quirk: lung smooth muscle expresses on its surfaces a protein that is the same as the bitter taste receptor. This could be useful, since they also discovered that activating that receptor with bitter substances causes the muscle to relax, opening up airways, and could represent a new way to treat asthma. That’s a fine discovery.

But man, it really tells us something about human psychology. I’m getting all this mail right now, and just about all of it asks the same question: Why do lungs have taste receptors? What is the purpose of sensing taste with the lungs? Even the investigators speculate this way:

Most plant-based poisons are bitter, so the researchers thought the purpose of the lung’s taste receptors was similar to those in the tongue — to warn against poisons. “I initially thought the bitter-taste receptors in the lungs would prompt a ‘fight or flight’ response to a noxious inhalant, causing chest tightness and coughing so you would leave the toxic environment, but that’s not what we found,” says Dr. Liggett.

Weird. I guess the teleological impulse really is etched deep into most people’s minds. I’m going to suggest that everyone just relax, let go, and embrace a simpler assumption.

There is no purpose.

That should be our default assumption. Gene regulatory networks are complicated, with expression of all kinds of genes coupled to other genes, so my first thought was that this was a simple biological accident, and totally unsurprising. I’ve looked at enough developmental gene expression papers to know that genes get switched on and off in all kinds of complicated patterns that have nothing to do with proximal function and everything to do with the network of connections between them; sometimes if gene A is active, the only ‘purpose’ is because A is coregulated by factor X which also switches on gene B, and B is the next step in a physiological or developmental program that is adaptive for the organism.

Another way to think of it: the handle on your teapot is wobbling loose, so you bring the home toolbox into the kitchen to tighten it up with your screwdriver. Your toolbox also contains wrenches and a hammer, but we don’t speculate that the reason you brought the hammer is that you need it right then to fix the teapot. The purpose of bringing the hammer is that it’s in the same handy toolbox as your screwdriver, which is not really a purpose at all.

Now the way evolution works is that this purposeless variation may fortuitously find a purpose — a gene in the T2R family of G-protein coupled receptors is uselessly misexpressed in the lungs, but a clever doctor finds a way to take advantage of it to treat asthma, or you may spot a vagrant mouse skittering across your kitchen counter, and suddenly the hammer becomes a useful implement of pest control — but the root of that innovation isn’t purpose, but purposelessness and serendipity.

There’s another reason to be unimpressed with the purpose of the expression of this gene in the lungs. Many of you may already be familiar with another quirk of the bitter receptor — its expression is variable in people. A common observation to make in genetics labs is the existence of non-tasters, tasters, and super-tasters to a substance called phenylthiocarbamide, or PTC. The mechanism of that is variability in this same kind of receptor gene now found to be expressed in lung tissue. Shouldn’t we be used to the random element of the expression of this gene by now?

Attenborough alert

Right now on Discovery…it’s First Life with David Attenborough, which is supposed to be about the origin of life on Earth. There’s a pretty severe metazoan bias, unfortunately, so it’s really about the origin of animals, but still it’s cool stuff about the Cambrian.

So that’s why Koch funded a major evolution exhibit

I was mystified why Chief Teabagger David Koch would invest so much in a Smithsonian exhibit on human evolution — usually those knuckledraggers object to people putting their ancestry on display. An explanation is at hand, though: his big issue is denying the significance of global climate change, and the exhibit is tailored to make climate change look like a universal good.

There are some convincing examples of the subterfuge being perpetrated. There is a big emphasis on how evolutionary changes were accompanied by (or even caused by) climate shifts, which evolutionary biologists would see as almost certainly true, and so it slides right past us. But, for instance, what they do is illustrate the temperature changes in a graph covering the last 10 million years, which makes it easy to hide the very abrupt and rapid rise in the last few centuries. They also elide over an obvious fact: we’d rather not experience natural selection. Climate change may have shaped our species, but it did so by killing us, by pushing populations around on the map, by famine and disease, by conflict and chaos. Evolution happened. That doesn’t mean we liked it.

I suppose it wouldn’t leap out at an evolutionary biologist because it is true: there have been temperature fluctuations and long term changes that have hit our species hard, and nobody is denying it. However, it’s a bit of a stretch to suggest that we should therefore look forward to melting icecaps and flooding seaboards and intensified storms. It’s probably also worth pointing out that our technological civilization is certainly more fragile than anything we’ve had before. The fact that we could be knocked back to a stone age level of technology without going extinct is not a point in favor of welcoming global warming.

Now we have a new question: how did this devious agenda get past the directors of the Smithsonian?

Bad evolution

There have been no science fiction movies that I know of that accurately describe evolution. None. And there have been very few novels that deal with it at all well. I suspect it’s because it makes for very bad drama: it’s so darned slow, and worst of all, the individual is relatively unimportant and all the action takes place incrementally over a lineage of a group, which removes personal immediacy from the script. Lineages just don’t make for coherent, interesting personalities.

io9 takes a moment to list the worst offenders in the SF/evolution genre. There are a couple of obvious choices: all of Star Trek, in all of its incarnations, has been a ghastly abomination in its depiction of anything to do with biology (I think you could say the same about its version of physics). Any episode with any biological theme ought to be unwatchable to anyone with any knowledge of the basics of the field; if you turn it off whenever it talks about alien races or whenever it mentions radiation from a contrived subatomic particle, though, you’d never see a single show. Gene Roddenberry must have been some kind of idiot savant, where the “idiot” half covered all of the sciences.

I’m very pleased to see that Greg Bear’s Darwin’s Radio gets mentioned for its bad biology. That one has annoyed me for years: Bear does a very good job of throwing around the jargon of molecular genetics and gives the impression of being sciencey and modern, but it’s terrible, a completely nonsensical vision of hopeful monsters directed by viruses and junk DNA. It’s also the SF book most often cited to me as an example of good biology-based science fiction, when it’s nothing of the kind.

TimeTree

People are always asking me for the source of those nice t-shirts that illustrate how long we’ve diverged from a given species. I think the name must be hard to remember: they’re at evogeneao.com. Now there’s a little software widget that will be just as neat-o.

Look up TimeTree, and remember to show it to the kids. This is a page with a simple premise: type in the name of two taxa (it will accept common names, but may give you a list of scientific names to narrow the search), and then it looks them up in the public gene databases and gives you a best estimate of how long ago their last common ancestor lived.

Grasshoppers and I, for instance, shared a many-times-great grandpa 981 million years ago. My zebrafish and I are practically cousins, with our last shared ancestor living a mere 454 million years ago. Hey, tree, we’ve been apart for 1407 million years, how’s it going? Sparrow! Long time no see! 325 million years, huh?

You get the idea. It’s great for getting the big perspective. The kids will pester you all the time for dates. Especially since…it’s got an iPhone app! Get on the App Store on your smart phone or iPad and search for TimeTree — it’s totally free (except for the cost of owning such a gadget, of course).

Oh, and once you’re done entertaining the children and yourself, it’s actually a serious tool. Tap on the results and it’ll take you to all the scientific details: breakdown of mitochondrial vs. nuclear date estimates, source papers, all that sort of thing.

For details on how it works, there’s also a published paper:

Hedges SB, Dudley J, Kumar S (2006) TimeTree: a public knowledge-base of divergence times among organisms. Bioinformatics 22(23):2971-2972.

Look, a cat! 92 million years.

Curl up and die already, HuffPo

Jebus, but I despise that fluffy, superficial, Newagey site run by the flibbertigibbet Ariana. I will not be linking to it, but if you must, you can just search for this recent article: “Darwin May Have Been WRONG, New Study Argues”. I don’t recommend it. It sucks. Read the title, and you’ve already got the false sensationalism of the whole story down cold.

It’s actually an old and familiar story that doesn’t upset any applecarts at all. There is a well-known concept in evolutionary theory of an adaptive radiation: a lineage acquires a new trait (birds evolve flight, for instance), or an extinction removes all competition and creates an opportunity for expansion (the dinosaurs are wiped out and mammals expand rapidly into vacant niches), and presto, new species and diversity abounds. For a really obvious example of this phenomenon, look to Darwin’s finches: one or a few species are storm-blown to an isolated chain of islands, and they gradually speciate to take on many roles.

See? No shock, no strike against evolution, or even against Darwin’s version of evolution. To claim otherwise is simply stupid.

Now the paper in question seeks to quantify the expansion of taxonomic diversity with the appearance of large-scale ecological opportunities, and concludes that competition and refinement by natural selection has not been the major driver of diversification, but that reason we have thousands of species of mammals and even more species of birds is more a consequence of chance and opportunity than strong competition. It’s a reasonable result, but not cause for a revolution; lots of us have been advocating for the importance of chance in evolution for many years, and it’s unsurprising that non-selective mechanisms of evolution will generate new diversity from a single species in an open, competition free field.

Bugger the awful Huffpo. One of the scientists, Sarda Sahney, has a nice blog with a sensible discussion of the paper. Read that instead.