Tuesday, December 26, 2006

The Evolution of Eyes Revisited

St. Jude researchers have identified gene Six3 as having a critical regulating role in the development of the eye lens in embryos. Six3, a transcription factor, is one of a network of such factors involved in regulating the development of eyes in vertebrates. Six3 activates another gene known as Pax6. Pax6 is believed to coordinate the functions of a group of genes working together to form the lens of an eye. As one researcher put it: "it puts the Six3 gene at the top of the genetic cascade that controls the development of the lens."

In Wilber and the Misunderstanding of Evolution arguments of well known evolutionists are presented which heroically destroy strawmen. Note this quote of Berra.

"Creationists [Wilber again?] frequently make the specious argument that an eye (or ear, wing, lung, etc.) could not have evolved because the intermediate stages would be imperfect and therefore not functional. They miss the point that a structure need not be in a final form to confer an advantage. Some vision is better than none. . . Eyes did not arise suddenly from nothing. They evolved gradually over hundreds of millions of years by incremental improvements over previous models...."

The incremental argument is familiar. Observing its application to actual developmental processes is not nearly so common. What were intermediate stages in the evolution of the regulatory cascade that includes the Six3 gene, the Pax6 gene and others? Of what advantage is a partially formed Six3 gene? Pax6 gene? How did a complex of regulatory elements evolve gradually? Why is it that defenders of mainstream theories spend their time attacking wind mills rather than addressing relevant biological systems?

9 Comments:

At 9:38 AM, Blogger umbjm said...

Nathan, you quoted:
"They miss the point that a structure need not be in a final form to confer an advantage."

This is true. Below, you conflate structures with genes.

"The incremental argument is familiar. Observing its application to actual developmental processes is not nearly so common."

It's incredibly common if you bother to read the primary literature.

"What were intermediate stages in the evolution of the regulatory cascade that includes the Six3 gene, the Pax6 gene and others?"

The Drosophila primary literature demonstrates the same cascades in less complex form. This is obvious even by reading the OMIM entries for the Six and Pax genes. Hint: The Drosophila genes don't have numbers at the end.

"Of what advantage is a partially formed Six3 gene?"

Nice straw man, Nathan. No one is claiming that there ever was a "partially formed Six3 gene." The multiple Six loci arose by duplication, so there's no evidence whatsoever that they were ever "partially formed."

"Pax6 gene?"

The same. Why do the mammalian numbers go up to 6, while flies have only one?

"How did a complex of regulatory elements evolve gradually?"

Duplication, Nathan.

"Why is it that defenders of mainstream theories spend their time attacking wind mills rather than addressing relevant biological systems?"

Unlike you, they do address relevant biological systems, Nathan. The evolutionary history of Hox genes is a well-studied subject that won't ever be covered in a St. Jude press release.

Why don't you read the primary literature instead of university press releases? You might get a significantly different picture of how real science is done in the real world. Heck, I'll bet that the St. Jude researchers cited much of this evidence (or at least reviews that summarize it) in their paper in EMBO Journal. Why not read it before blogging about it?

 
At 10:08 AM, Blogger William Bradford said...

"How did a complex of regulatory elements evolve gradually?"

Duplication, Nathan.


That does not answer the question. It's more like an incantation lacking details. And it should be in plural form. Duplications. Complexes are not solo acts and their origin is inferred, not observed.

 
At 10:40 AM, Blogger umbjm said...

William wrote:
"That does not answer the question."

Sure it does. It also corrects Nathan's misconception about a partially formed gene.

"It's more like an incantation lacking details."

I pointed Nathan to the details.

"And it should be in plural form. Duplications."

I was using it as a verb. The answer to a "how did something [verb] is obviously a verb.

"Complexes are not solo acts..."

Obviously. What's your point?

"... and their origin is inferred, not observed."

Again, what's your point? At least the predictions that flow from evolutionary inferences are tested empirically.

 
At 3:53 PM, Blogger Nathan Munson said...

At least the predictions that flow from evolutionary inferences are tested empirically.

Such as this one: Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein

 
At 4:06 PM, Blogger umbjm said...

Yes, like that one. Why didn't you answer my questions?

 
At 5:07 PM, Blogger Nathan Munson said...

How does this support standard theory?

"As observed in computational systems, negative epistasis was tightly associated with higher tolerance to mutations (robustness). Thus, under a low selection pressure, a large fraction of mutations was initially tolerated (high robustness), but as mutations accumulated, their fitness toll increased, resulting in the observed negative epistasis. These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness. Threshold robustness is inherently epistatic—once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed."

 
At 11:22 PM, Blogger umbjm said...

It's not inconsistent with MET. It contradicts a model (or a hypothesis), not any theory.

If you ID folks don't want to be lumped together with creationists, why do you conflate theories with hypotheses just like they do?

And why are you afraid to answer my questions?

 
At 12:00 PM, Blogger William Bradford said...

One of the earmarks of complex objects known to be intelligently designed is, not that they function outside natural laws, but rather that natural laws alone are insufficient to generate them. Accordingly, a fragile stability threshhold would support a model for intelligent causality relevant to the protein fitness alluded to.

 
At 10:18 AM, Blogger umbjm said...

So if, as Nathan seems to be implying, this is inconsistent with evolutionary theory, and as you say, supports "a model for intelligent causality," did any IDer predict this?

And what is your model for intelligent causality?

 

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