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« Okay, I Confess, Although Sahotra Had to Beat It Out of Me: I Hold the Position I've Always Held (Commentary on Sarkar v. Nelson Debate, pt 1) | Main | Intelligent Design and Earwax »

Junkyard Dog Chases Texas Philosopher (Commentary on Sarkar v. Nelson Debate, pt 2)

Since Sahotra Sarkar has now confirmed that he thinks I am toothless (see his post for March 17), I am happy to show him the exact function of mammalian canines.

Given the format of our recent (March 9) debate at UT-Austin, we had little opportunity to respond to each other directly. Sahotra already told me in person that he thought I got away with murder that evening. Judge for yourself when the Undergraduate Philosophy Association (UPA) video is available on the web.

So -- back-and-forth blog posts for a while. I’ll have two other entries to this series; today, I want to look at a couple of points that came up during the debate, and also to respond (in part) to Sahotra’s latest post about the event.

1. How evolutionary biology got a bad reputation

“In science's pecking order,” wrote University of Chicago evolutionary geneticist Jerry Coyne, “evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics.” [1] Coyne attributed this low ranking to the inescapable historical dimension of evolution: it’s hard to test theories about events that occurred hundreds of millions of years ago. In my experience, however, dealing with history isn’t the real reason evolutionary biology suffers.

Evolutionary biologists themselves are to blame. They abuse their own theory, waving phrases such as “selective advantage” at the phenomena like magic wands, often in the complete absence of any genuine biological understanding about the puzzle at hand. As a result, evolutionary theory decays into a collection of untestable or mutually contradictory tales. College biology students endure just enough of these tales to satisfy the bare minimum of departmental requirements. Then they get the hell out of Darwin.

Q. Ever wonder why organizations such as the American Society of Naturalists regularly complain that molecular biology graduate students (for instance) don’t know much, or any, evolutionary theory?

A. Students don’t see the point of storytelling. They could take a Fiction Writing course for that.

Here’s an example from the debate. During the Q & A, I pointed out that classic evolutionary predictions about homology had been refuted by widespread incongruities between developmental pathways and anatomical endpoints. According to the classic prediction, the best criterion for anatomical homology is “similarity in developmental history,” meaning that homologous adult structures, such as the gut in all vertebrates, should develop via homologous pathways and from homologous precursors. [2]

Except they don’t:

Alimentary canals [the gut] are homologous throughout the vertebrates, arising from endoderm with an ectodermal component at stomodaeum and proctodaeum. Nevertheless, the alimentary canal forms from the floor of the embryonic gut cavity in lampreys and urodele amphibians, from the roof of the cavity in sharks, from both floor and roof in anuran amphibians, and from blastodermal hypoblast in birds and reptiles. [3]

Telling moment: as I was explaining this, the two UT-Austin biologists on the faculty panel exchanged a look of surprise, which could only have meant “Did you know that?” I hope the UPA videotape captured their expressions.

My response to these data was design-theoretic. Maybe the correct explanation for the anatomical similarity of the gut in vertebrates is not historical (i.e., the gut evolved once in the common ancestor of all vertebrates, and all vertebrates inherited this form), but functional. A vertebrate gut needs to be a long, two-ended tube with an extensive epithelial surface for extracting nutrients, but that tube could be constructed developmentally in any number of ways (as it is). In any case, unlike naturalistic evolution, design is not committed to material (common) descent, so these striking developmental patterns don’t speak against ID as they do against nauralistic evolution.

No problem for Sahotra, however. Natural selection, he said, simply preserved the adult anatomy -- keep a tube -- while allowing the developmental pathways to vary. Where’s the puzzle? Evolution triumphs again.

The charitable description for that explanation is “ad hoc.” The accurate description is the steaming organic matter, suitable for fertilizer, produced by the nethermost regions of a male bovine.

Could Sahotra provide any experimental evidence, from any vertebrate group, that developmental pathways for whole organ systems (such as the gut) varied as significantly as his selection story requires? No -- the usual term for such variation is “embryonic lethal.” Faced with data that refute the neo-Darwinian account of homology, Sahotra told a Tall One, abusing the theory of natural selection in the process.

In a chapter I wrote on natural selection that I sent to Sahotra before the debate, I repeated a point that Richard Lewontin (one of Sahotra’s mentors) has stressed throughout his career: appeals to natural selection as the causally implicated mechanism for any change require evidence of relevant variation. There is no observational or experimental evidence, however, for the large-scale change required to radically shift the developmental pathway of an entire organ system in a vertebrate. Thus, using selection to “explain” in this case amounts to no more than waving a magic wand. As Michael Lynch argued in a recent paper, “an uncritical reliance on adaptive Darwinian mechanisms to explain all aspects of organismal diversity is not greatly different than invoking an intelligent designer.” Intelligent designer, in Lynch's lexicon, is not a term of praise.

I heard other Tall Ones that night. For instance, in my presentation I talked about the world-class puzzle of “orphan” (or ORFan) genes, which deserve to be much better known and studied than they are. Orphan genes -- open reading frames with no detectable similarity to any other known sequence -- constitute a surprisingly high percentage of the genomes of fully-sequenced organisms. Their origin is currently mysterious. I've argued that, in conjunction with other, longer-standing problems, orphans may provide strong motivation for design-theoretic approaches to organismal diversity.

But the response of the biologists in the UT-Austin discussion was to shrug. Orphans. Yeah, so what. As Sahotra put it, "orphan genes pose no looming problem over evolution." In a discussion at a bar with Dan Bolnick and me, Sahotra again waved off the problem as insignificant and readily explained by current theory:

Later in the night, when Bolnick and I began constructing several plausible scenarios for the evolutionary emergence of such genes, all Nelson had to say is that he would think about it.

Sahotra, I was being polite. In my experience -- which, with respect to orphan genes, you and Dan abundantly confirmed -- when evolutionary biologists are confronted with an observational puzzle, the first thing they do is to throw an untestable story at it. Or several such stories, burying the problem under a steaming pile of speculation. What anomaly, Paul? We just solved that problem for you. [By contrast, when Dan described his own research with fish, I found his arguments precise and compelling.]

No. You told me a bunch of Tall Ones, mostly involving those familiar non-specific actors Time, Chance, and Some Ill-Defined Process. An empirical approach to ORFans would ask, What are these genes (and their protein products), what are they doing, how are they distributed among different groups, in what cases are they essential, what are the known (i.e., experimentally well-supported) mechanisms for the origin of novel proteins, and so on.

You and Dan spun some on-the-spot tales, to which the only polite response was silence. Or what I said that evening: “OK, I’ll think about that” (yes, for about one second, while saying to myself, gee these guys need to get up to speed on the relevant data).

2. Sahotra says that he doesn't take ID seriously.

No, of course not. Which is why he just wrote a ten chapter book about the topic. [4]

OK, no joking: I know what Sahotra means when he says that he doesn't take ID seriously. He means (a) ID shouldn't be taught in public schools any time soon [I agree and don't care about that], but more importantly, (b) no biologist should modify his or her research program to incorporate ID or even to think about it.

That's fine with me. It's not the responsibility of the conservative majority to take up the ideas of the radical minority.

But the majority needs to guarantee that the ordinary rules of scientific or academic discourse are respected for the minority as well. Sahotra was puzzled that I talked about censorship and academic freedom as much as I did at the debate. He asks:

Now, when was the last time any of you heard that anyone had suggested that creationism should be censored (and not merely that it shouldn’t be presented as accepted science)?

Tomorrow, I will send Sahotra by registered mail documentation of an unquestionable case of the academic censorship of intelligent design, at the university level. Let's see what he says about it.

REFERENCES

1. Jerry Coyne, The New Republic, 3 April 2000.

2. A.S. Romer & T.S. Parsons, The Vertebrate Body (Philadelphia: Saunders, 1977), p. 10.

3. Brian Hall, "Homology and Embryonic Development," Evolutionary BIology 25 (1995):1-37; p. 14.

4. Sahotra Sarkar, Doubting Science? On Creationist Designs on Evolution. This book promises to be provocative and readable.


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