Intelligent Design creationists unable to grapple with the substance. Surprise!

Uncommon Descent linked to my criticisms of the Biology of the Baroque, Intelligent Design creationism’s latest misconception, that biologists believe every detail of every organism is the product of natural selection…but they didn’t bother to quote any of my criticisms. It’s weird. They could have quoted the gist of my complaint:

So evolution should produce only the biological equivalent of sterile gray Soviet architecture, and if you find something that is the equivalent of a Baroque church, then evolution is refuted. This entire argument is built around what Michael Denton calls the fundamental assumption of Darwinism…that all novelties are adaptive. To which biologists around the world can only say, “Fu…wha?” in total confusion. That is not one of our assumptions at all. Novelties are going to arise as a product of chance mutation; if they are not maladaptive (and sometimes even if they are), they can spread through a population by chance-driven processes like drift. And some elaborate fripperies can acquire a selective advantage, like that example of Soviet architecture, the peacock’s tail, which this video actually uses as an example of non-adaptive order.

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Michael Egnor is business as usual for creationism


The other day, I wrote about how New Atheists are the same as the Old Atheists, and in particular, how all kinds of atheists are responding to the failure of all religion to answer basic questions about our existence. I could argue that religion is a font of bad ethics, bad philosophy, bad charity, etc., but because I’m a science guy I wrote about how badly it addresses questions of our origin and nature, and how the major premises of all religions are false.

This has roused the indignant jellyfish of the Discovery Institute, Michael Egnor, who has declared that atheism is a catastrophe for science. The most remarkable thing about his complaint is that I asked a number of questions about key premises of faith, like about the existence of a deity, an afterlife, and why we should believe your particular dogma over another, and he doesn’t answer any of them. He doesn’t even try. This isn’t even an argument.

I ask, “Why should I believe one religion over another?”

He harumphs back, Because Christianity is obviously true.

I could ask, “How do you know?”

Because it just is.

This is not a productive direction the discussion could take, but it’s what I expect from a Discovery Institute flunky. The details are not much different from my broad outline. So I bring up this basic question in my post:

Why should I believe in any god? We don’t need an intelligent authority to explain the universe…

His answer:

Of course we need an intelligent authority to explain the universe. The universe is shot through with intelligibility. Nature is governed by astonishingly complex and elegant physical laws, and the laws themselves are written in the language of abstract mathematics. In fact, theoretical physicists must often explore utterly new mathematical theories in order to explain the behavior of inanimate matter.

That’s not an answer. Nothing in that addresses the issue, and when he continues on to babble about the religious beliefs of scientists, claiming that many of them have believed in gods, he is mistaking personal quirks that are irrelevant to question for the facts that support his contention. I could argue that many scientists have been good musicians, but it would not imply that therefore my theory that the universe began with a note on a violin is true; an even more universal truth, that all scientists have possessed nostrils, is not support for my theory that the Big Bang was actually the Big Sneeze. And doesn’t Sandwalk’s list of atheist scientists immediately refute the idea that religiosity is a precondition for good science?

Egnor is simply making a fallacious assertion, and is begging the question. I will reply with a quote from Percy Shelley, published in 1814, which the Intelligent Design creationists will ignore, as they’ve been doing for two centuries.

Design must be proved before a designer can be inferred. The matter in controversy is the existence of design in the Universe, and it is not permitted to assume the contested premises and thence infer the matter in dispute. Insidiously to employ the words contrivance, design, and adaptation before these circumstances are made apparent in the Universe, thence justly inferring a contriver, is a popular sophism against which it behoves us to be watchful.

It’s Paul Nelson Day, again


Solemn greetings, all. Today, as the more reverent among you know, is Paul Nelson Day. Today is the 12th annual feast day of St Nelson, patron saint of obtusity and procrastination, and we honor his contributions to science by…well, by not doing much of anything at all. You could make grandiose claims today and promise to make good on them tomorrow, a tomorrow that stretches out into a decade or more, I suppose, but that’s too much work. Instead, maybe we should all just shrug and say we’ll think about celebrating later.

Oh, jeez, shrugging? I don’t have time for that. How about if we don’t and just say we did.

I also thought about suggesting waffles as the perfect food for this day, but nah, I’d have to cook them, or go to a restaurant. I’m just going to say “waffles!” and put it off to some other day.

Anyway, if you don’t know the story, Paul Nelson is a creationist who attended the Society for Developmental Biology meetings in 2004, with a poster in which he claimed to have developed this new evo-devoish parameter, Ontogenetic Depth, that supposedly measured the difficulty of developmental complexity to evolve. I quizzed him on it, and specifically asked him to explain how I could measure it in my zebrafish, for example, and he couldn’t tell me, even though he seemed to be saying that he and a student had been doing these ‘measurements’. But he promised to send me a paper he was working on that explained it all. Tomorrow! A tomorrow that never came.

So now we remind him of his failure every year. It’s a good thing to point out to Intelligent Design creationists that they don’t seem to be very good at fulfilling their grand promises.

He seems to sometimes notice that he’s being mocked, at least. Last year, he tried to trot out Ontogenetic Depth 2.0, which was just as impractical and ill-conceived as the first non-existent version. Maybe he’ll have a new beta for us this year, too?

Unlikely. Too much work. Not in the spirit of the day.

Your exactly accurate definition is still exactly stupid


One of the most common dodges used by Intelligent Design creationists is to use a vague definition of their subject so that critics have nothing specific too attack, and also so they can accuse anyone who disagrees with them of using a strawman argument. For example, they claim that organisms exhibit “specified complexity”, which cannot have evolved and requires a designer. If someone rightly points out that their definition of complexity is nowhere close to what real complexity theorists use, they can say, “Ah, but I’m talking about specified complexity, which is something different,” which leaves you adrift and wondering what the hell they’re talking about. I read that whole ghastly tome by Meyer titled Signature in the Cell, and he throws around that phrase willy-nilly and never bothers to define “specified”.

Now David Klinghoffer is complaining about Lawrence Krauss’s performance in a recent debate, claiming that he mischaracterized ID creationism horribly. Nowhere in the post does he tell us what Krauss said, and he’s also not quoted in the creationist post he’s citing, which is weird and annoying because they’ll just use the ambiguity to weasel away some more, but Klinghoffer does approve a given definition of ID creationism, saying this is exactly accurate.

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Axon guidance mechanisms are thoroughly evolutionary in origin

The Discovery Institute thinks axon guidance mechanisms are evidence for intelligent design. I think they just trawl the scientific literature for the words “complex” and “purpose” and get really excited about the imaginary interpretations in their head of papers they don’t really understand.

There’s no mention of evolution here, nor in the full paper in Science. The paper, however, does use a notable word: purpose. “These findings identify NELL2 as an axon guidance cue and establish Robo3 as a multifunctional regulator of pathfinding that simultaneously mediates NELL2 repulsion, inhibits Slit repulsion, and facilitates Netrin attraction to achieve a common guidance purpose.” In fact, they use it again in their concluding sentence:

Our results also show that Robo3.1 serves as an integrative hub: Its three diverse actions in response to three different cues — mediating NELL2 repulsion from the motor column, potentiating midline Netrin-1 attraction, and antagonizing midline Slit repulsion — act simultaneously, are mutually reinforcing, and serve the common purpose of steering commissural axons toward and across the midline. This multiplicity of mechanisms likely helps ensure high-fidelity steering of axons to their targets.

It’s one of those occasions in biology (not rare) when the term “intelligent design,” despite other merits, falls flat as a description. This is super-intelligent ultra-design.

Getting axons in the nervous system to their proper destinations actually is a very complex problem: much wires, many connections, wow. If you look at complex systems like the brain, you shouldn’t be surprised that the mechanisms are complex. And further, the functional requirements of those systems, which may require that Neuron A navigate to Target B in order for the pattern to work, it’s easy to say that the purpose of those mechanisms is to hook A up to B. It does not imply the existence of a designer, only the existence of functional constraints.

But also, they picked a system with which I’m fairly familiar. Way back in the 1990s, this is what I did: try to figure out the rules behind commissural neuron migration, the very stuff the DI is talking about. I was focusing on a cellular approach — I was observing neurons that grew across the midline to contact cells on the opposite side of the nervous system — and I reached some of the same general answers that more recent research has discovered. The question was why an axon would grow all the way across the nervous system to reach a target that had a closer equivalent right next door, on the same side.

Here’s a simple cartoon version of the problem. Neuron A is supposed to, has the function of, has the purpose of connecting to Neuron B; in the normal animal, it grows all the way across the midline to touch the contralateral (on the opposite side) B neuron.


But the question remains: there’s a left B and a right B. Why doesn’t neuron A on the left side take the lazy shortcut and grow straight to the left B?


The answer we came up with in my work is that there is a hierarchy of interactions. That A finds the midline much more attractive than B at first, so it grows to the middle of the animal, and then, after a brief flirtation with the midline, changes its priorities to favor B cells after all, and just keeps growing across the midline to find the other B. (Actually, what we found that was most important in changing the left A’s affinities was contact with the right A, which arrived at the midline at about the same time.)

We worked that out with direct observations of neuron behavior, and also a series of experiments in which we killed various cells A would interact with. What we didn’t know at all was what molecules were involved.

And that’s where the Discovery Institute is so wrong. We had a cellular description, but when other laboratories in the late 1990s started discovering the molecular signals involved, molecules like Netrin and Robo and Slit, it was a wonderful revelation. It’s like how on one level, you can see a car and watch it run and figure out general things like wheels and steering, but when you get out the wrenches and start taking the engine apart, you can really see the mechanistic basis of its operation. Every step deeper into the guts of the problem tends to reinforce our understanding that it’s fully natural, and was built around natural processes.

The other big shift was that we could now generalize to other organisms and pick apart the evolutionary foundations to these mechanisms. I was looking at specific cells in the grasshopper embryo, and we could see that those very same cells are present in other arthropods, but we didn’t have the tools to do molecular comparisons. Identifying the molecules responsible meant that we could ask if they were present in other organisms, whether they were conserved, and whether these molecular processes were used in multiple cells, rather than just the few I studied.

If the Discovery Institute had looked just a little bit harder (or had not intentionally chosen to ignore all the papers that studied the evolution of axon guidance mechanisms), they might have noticed that there’s a very interesting literature on how these molecules evolved. There are plenty of papers that survey the evolutionary pattern of axon guidance mechanisms.

When did axons and their guidance mechanisms originate in animal evolution? Many axon guidance receptors (e.g. type II RPTPs, Eph RTKs, and the DCC, UNC5 and Robo families) are related to CAMs of the immunoglobulin superfamily, suggesting that axon guidance mechanisms evolved from signaling pathways involved in general cell–cell or cell–ECM adhesion in an ancestral animal. The simplest animals with nervous systems are cnidarians, which have isopolar neurons arranged in ‘nerve nets’; simpler animals (e.g. sponges, mesozoans) have no recognizable neurons. Thus, neurons and their guidance mechanisms must have evolved in a common ancestor of all metazoans, but after the divergence of sponges (Figure 1). Intriguing recent work suggests that sponges, which have no discernible nervous systems, nevertheless contain a diverse set of receptor tyrosine kinases and RPTPs [54,102]. Thus, many of these molecules could have evolved prior to (and may have been necessary for) the evolution of nervous systems in the urbilaterian.

Many axon guidance mechanisms are not only conserved at the molecular level, but also at the level of the body plan (reviewed in [103]). For example, netrins are secreted from ectodermal cells at the ventral midline of nematodes and insects and from the floorplate of the spinal cord of vertebrates (dorsal midline ectoderm, homologous to the ventral ectoderm of insects). Thus, in an ancestral animal, circumferential movements of axons or cells around the dorsoventral axis were probably oriented towards or away from a midline netrin source, and perhaps also from a midline Slit source. Studies in the coming years are likely to reveal the extent to which the patterning roles of other guidance mechanisms have been retained during the evolution of different body plans, and may help further outline the likely organization of the nervous system of our primitive ancestors.

These molecules are also multi-functional and play roles in other systems than the nervous system. They’re important in organogenesis and the maturation of the reproductive system, and are part of an interactive network of cell signaling molecules. It’s really complex, but what the DI doesn’t appreciate is that biology and evolutionary processes are really, really good at generating complexity. Look ot all the things the SLIT-ROBO system does!


You might notice that they play a role in cancer signaling, too, but then everything does.

Once again, the Intelligent Design creationists completely miss the point. The work on these axon patterning systems has been deeply informed by evolutionary perspectives, while the DI is reduced to mining for mentions of “complexity” in papers, as if that somehow supports their ignorance-based position.

Chisholm A, Tessier-Lavigne M (1999) Conservation and divergence of axon guidance mechanisms. Curr Opin Neurobiol. 9(5):603-15. (Note that this paper came out very shortly after the discovery of netrins, by the fellow who discovered them — evolutionary biology has been part of this story from the very beginning.)

Dickinson RE1, Duncan WC (2010) The SLIT-ROBO pathway: a regulator of cell function with implications for the reproductive system. Reproduction 139(4):697-704.

Casey Luskin vs. Homo naledi

The Intelligent Design Creationists are always getting annoyed at the third word in that label — they’re not creationists, they insist, but something completely different. They’re scientists, they think. They’re just scientists who favor a different explanation for the diversity of life on Earth than those horrible Darwinist notions. But of course, everything about them just affirms that they’re simply jumped-up creationists with airs, from their founding by an evangelical Christian, Phillip Johnson, to their crop of fellows like Paul Nelson and William Dembski, who happily profess their science-denying faith to audiences of fellow evangelicals, to their stance on every single damn discovery that comes out of paleontology and molecular biology. The real misnomer is that they work at a think-tank called the Discovery Institute, when their response to every scientific discovery that confirms evolution is a spasm of jerking knees and a chorus of “uh-uh” and “no way”.

It makes no sense. They completely lack an intellectual framework for dealing with new findings in science, so instead of explaining how Intelligent Design “Science” better explains an observed phenomenon, they instead dredge up some entirely unqualified spokesperson to mumble half-baked, pseudo-scientific excuses for why those Darwinists have it all wrong.

Case in point: Homo naledi, the newly discovered South African species. If they actually were Intelligent Design “Scientists”, they’d respond with the same puzzled happiness that real scientists do: we’re not sure where to place this species in our family tree, but it’s very exciting, and fits with our growing knowledge about the diversity of early hominins — there were lots of different species of human ancestral species and dead-end branch species living at the same time on Earth right up to less than 100,000 years ago. This fact of the fossil data has been known since I was a wee young lad growing up reading about Louis and Mary Leakey in National Geographic. That multiple hominin species coexisted and overlapped in time is part of the body of data that we have, and it fits just fine with evolutionary theory. The history of a lineage is a braided stream, with populations branching off and diverging, sometimes dying off, other times merging with other branches. And we explain this pattern with theories about common descent, genetic drift, and selection.

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2 + 2 = 17, for certain values of 2

A while back, I responded to Behe/Luskin’s claim that his model proving the impossibility of evolution of chloroquinone resistance was vindicated. I pointed out (as did Ken Miller) that showing that a particular trait required multiple point mutations did not affect the probability in the naive way that Behe and Luskin calculated — in particular, it did not require that the mutations be simultaneous. We’re familiar with a great many known mutations that involve multiple sequential hits to have their effect. I mentioned the work on steroid receptor evolution, and how cancer is an amazing example of the power of the accumulation of sequential variants.

Behe fired back, issuing a challenge to ‘show my numbers’. If he could have said anything to confirm that he was obliviously ignoring my point, that was it, and so I blew him a raspberry and ignored his challenge. I wasn’t arguing with his numbers, and we could even use his very own set of numbers — my point was in the operation he was doing with those numbers. His assumption is that you must have two mutations occur simultaneously, in the same individual, so that you simplistically multiply the probabilities together to get an improbably low frequency. I’m saying that’s invalid: these mutations can happen independently, they can accumulate to some frequency in the population, and then a second mutation can occur.

Now Larry Moran has carried through on the calculations. Using the known data on mutation rates, and throwing away Behe’s bogus demand that everything occur in the very same instant, he shows that the evolution of chloroquinone resistance ought to be rare, but not at all impossible, and with frequencies that are in the ballpark of what is observed.

Furthermore, Moran describes a paper that quantifies the presence of malaria strains in the population that contain pieces of the resistant combinations and that further describe the sequential series of mutational events that led to the most resistant strains.

All of the strains (except D17) are found in naturally occurring Plasmodium populations and the probable pathways to each of the major chloroquine resistant strains are shown. It takes at least four sequential steps with one mutation becoming established in the population before another one occurs.

None of the mutations occurred simultaneously as Behe claimed in his book.

The intelligent design creationists are somehow still crowing victory. I don’t quite understand how — their premises have been demolished, they’ve been cut off at the knees, but I guess their followers are easily bamboozled if they shout “math!” loud enough. Even if the math is wrong.

There’s a secular argument for wearing underpants on your head. So?

Sarah Moglia points out that David Silverman has been saying some weird things recently.

Yesterday, an article was published about atheists at CPAC (Conservative Political Action Conference). Featured prominently in the article was Dave Silverman, president of American Atheists. In it, Dave was quoted as saying, “I will admit there is a secular argument against abortion. You can’t deny that it’s there, and it’s maybe not as clean cut as school prayer, right to die, and gay marriage.” Is that so?

I’m trying to figure out what this ‘secular argument’ actually is; he didn’t say. I have encountered anti-choice people tabling at an atheist convention, and they couldn’t say either — I got the impression these were actually religious people trying to evangelize to the atheists with a pretense, and they stood out oddly from the rest of the crowd…rather like an atheist shilling at CPAC. So speak up, Dave, tell us what these secular arguments are.

I’m also wary because in my business we’ve run into folks peddling religious bullshit under the guise of being secular before: we call them intelligent design creationists. No one is fooled. Similarly, the anti-choicers who claim to be making a rational secular argument are easy to see through, since they ultimately always rely on some magical perspective on the embryo.

But here’s the bottom line: it is not enough to make a purely secular argument. It has to also be a good argument, unless atheism is to become a smokescreen for nonsense, to be accepted purely because of its godless label. And then atheism might as well just be another religion.

Magic RNA editing!

One of those wacky Intelligent Design creationists (Jonathan McLatchie, an arrogant ignoramus I’ve actually met in Scotland) has a theory, which is his, to get around that obnoxious problem of pseudogenes. Pseudogenes are relics, broken copies of genes that litter the genome, and when you’ve got a gang of ideologues who are morally committed to the idea that every scrap of the genome is designed and functional, they put an obvious crimp in their claims.

So here’s this shattered gene littered with stop codons and with whole exons deleted and gone; how are you gonna call that “functional”, creationist? McLatchie’s solution: declare that it must still be functional, it’s just edited back into functionality. He uses the example of GULOP, a gene responsible for vitamin C synthesis, which is pretty much wrecked in us. Nonfunctional. Missing big bits. Scrambled. With missing regulatory elements, so it isn’t even transcribed. No problem: it’s just edited.

As I mentioned previously, the GULO gene in humans is rendered inactive by multiple stop codons and indel mutations. These prevent the mRNA transcript of the gene from being translated into a functional protein. If the GULO gene really is functional in utero, therefore, presumably it would require that the gene’s mRNA transcript undergo editing so that it can produce a functional protein. It’s not at all difficult to understand how this could occur.

Yes, RNA editing is a real thing. RNA does get processed before it’s translated into protein. McLatchie has a teeny-tiny bit of knowledge and is abusing it flagrantly.

I’ve hammered out dents in a car, and I’ve touched up rust spots with a little steel wool and a can of spray paint. My father was also an auto mechanic and could do wonders with a wrench. Auto repair exists, therefore…


…patching up that vehicle should be no problem at all, right? I expect to see it cruisin’ down the highway any time now.

Maybe two cans of spray paint this time…?