Random Degradation

A good article? This article is non-sense. It just shows once again that DaveScot has no grasp on evolutionary theory at all. Alas, if you think this is a good article, apparently neither do you.

Unfortunately many biologists are still uncomfortable with quantitative analysis (many, in the same mood as the above post by Ric, simply sweep it aside as “nonsense” – even when they don’t have a clue what was actually said).

All sciences must fall to mathematics. Qualitative analysis, the prime mover of all biology, is insufficient and constitutes little more than large scale ignorance (perhaps I shouldn’t be that mean – qualitative analysis does have limited uses; it is just entirely inappropriate for large scale extrapolation like Darwinism).

Nathan,
The article may not be quite nonsense, but it is not all correct and reflects a very narrow interpretation of the mutation process. There are tw9o things I don’t agree with:
1. DaveScot claims that mutations do not occur randomly. If he means that the probability of a mutation in one genomic locus is not the same as in another locus on the genome, he is probably technically correct, but not for the reason he states (or I understand him to mean). We know from the literature that there are sites on the human genome that are more prone to undergo mutational damage than others. So these sites do have a higher probability of being mutated than others. However, the mutation process is still random in the sense that is it is a probabilistic process and cannot be predicted when it occurs.
2. More to the point, DaveScot tries to downplay the possible contributions of beneficial mutations, pointing out that most mutations, if they are not detrimental, are neutral but virtually never beneficial. As evidence he has, in the past and to a certain extent here, mentioned mutational experiments with bacteria and yeast to which he refers as “directed change” (and that is where the work “nonsense” applies). Bacteria have a mechanism where under certain stress conditions, an error-correcting mechanism is suppressed. This has the consequence that the number of copying errors upon cell division increases and the daughter cells have a higher probability of possessing a mutation somewhere. If I understand him correctly, he sees a telic mechanism behind that, in that this is not a process leading to randomly occurring mutations, followed by selection according to the environmental stress that has been inflicted. As if the bacterium was ready for this stress and consequently adapted purposefully. There is absolutely no evidence that demands this interpretation.

That is why I provided my example of HbS in that thread. There is no evidence for any induction of mutagenesis in higher organisms, and in fact the mutation that leads to the detrimental sickle cell disease, is beneficial under other conditions. There was no purpose for this mutation. As far as we can tell, this type of mutation happens with the same probability in all human populations. The only difference is that selection in geographic regions of malarial infections has led to a significant increase in the fraction of the population that carries this mutation. That is a clearcut case of random mutation followed by natural selection, nothing else.

Ofro,

You make a valid point. The functional/selectional relationship between the genome and environmental pressures is very fluid, because the environment is in a constant state of flux. For this reason natural selection will not always maintain even fully functional metabolic pathways, because shifting environmental pressures will alter that relationship.

I will add that his point is often correct though, because if any specimens in the population still have the original genetic material after the environmental pressures reverse (if they do), the population will drift right back to its initial state (or near so).

As my comment suggested on the original article though, the ID platform actually benefits from such a demonstration of “beneficial” mutations as Hemoglobin s. Bottom line is that it still serves as a reduction in CSI. As DaveScot points out, re “arrival of the fittest,” Darwinism still provides no mechanism for producing the initial genetic state (from which the “beneficial” derivatives you speak of were derived).

-Matthew