One step too far. Behe once collaborated with snokes to computationally test the EoE hypothesis with a simulation. Two papers were published in Protein Science. They were later retracted. I am not sure they should have been retracted.
I was thinking in terms of feasibility, and the cost dynamic. Perhaps difficulty is the wrong word. But I usually associated the word with feasibility. For example, if I tell my senior, it’s difficult to do a project, it will be because of feasibility issues.
How do you guys understand the term difficult in your projects?
Maybe some others can chime in here, but the following excerpt from Behe’s latest response to Lenski seems to be saying (or predicting) that all genes under positive selection will inevitably be “broken”. That seems to me to be both preposterous and testable.
As I initially discussed in a book chapter and as I emphasize in Darwin Devolves , beneficial degradative mutations have a very strong, natural, built-in advantage over beneficial constructive ones, exactly because of their frequency of occurrence . Let me explain briefly here. Consider two genes, either of which when mutated would be beneficial for an organism to meet some particular selective challenge. The first gene (call it A ) would be helpful if it mutated (call the mutated protein A*) at a particular residue of the protein it coded for to give a new constructive feature (perhaps a helpful new binding site). The second gene (call it B ) would be helpful if it mutated (to B*) so that its activity were substantially degraded or eliminated entirely. Yet there are orders of magnitude — a hundred to a thousand — more ways to degrade B than to improve A . That means that if neither mutation were originally present in the population of a species, B* would be expected to appear in only a hundredth to a thousandth of the time needed for A* to show up. For example, if in this situation the time expected for a constructive mutation to arrive were a hundred thousand years, a degradative mutation would arrive in only one hundred to one thousand years. The result is that B would have 99,ooo to 99,900 years to spread through the population to fixation before A* even showed up.* If both A* and B* relieve the same selective pressure, then when A* eventually did show up there would be no more pressure to relieve, since B* had done so long before. Thus B* has a built in advantage simply because it is degradative — because its mutation rate is much higher.
If a population is large enough to be expected to already contain some copies of A* and B*, then, simply because of the many more ways to break B to produce B*, there would be expected to be a hundred to a thousand times the number of the broken gene in the population compared to A*. That means it would have a hundred to a thousand times the chance of fixing before A*. Looking at it from a different angle, the selection coefficient for B* could be a hundred to a thousand times less that for A* and still have an equal chance to fix in the population first — to fix a degraded gene.
Lets not play word games here. Its a simple question. I will split it to make it easier -
a)Can an experiment be devised that will “test” Behe’s hypothesis about ApoB in Polar bears.
b) Is it feasible to do such an experiment.
The Lord giveth… and He taken away. You did so well with @Greg, and now you are plotzing …
Behe is “taking Evolution to task” for BEING Evolution. So of course there is a test about ApoB… with only one exception: there is no test that will tell us whether God is “ignoring” the polar bear testing … or is helping with the polar bear testing.
And this is the fundamental problem with Behe’s whole book! There is no fathomable way to distinguish whether a land mammal “devolved into a whale” because God was ignoring it … or because God intentionally wanted a “devolved mammal” as a whale!
And you, my dear @Ashwin_s, will never have answer to this question… nor will Behe.
If this is your only argument against Behe, I have bad news.
Knockout mouse studies on the APOB gene also produced confusing results: two-thirds of male ApoB heterozygous mice were found infertile, despite normal genitourinary system function and mating behavior (Huang et al, 1995). Contrary to the above studies, infertility was not reported in the study by Farese et al (1995) on APOB heterozygous male mice. Our study concludes that the APOB gene deletion polymorphism is not a risk factor for the development of infertility in Indian men
Studies were done on humans, especially Indian Men did not find the same effect. From which We can conclude that maybe sometimes infertility might occur in male mice with deficient APOB gene, but you cannot directly extrapolate to other species.
Hence, this conclusion is inadequate and needs to be experimentally verified. If you have not done an experiment to prove this you cannot blame Behe.
If the polar bear mutations acted to lower the activity of its own APOB, results similar to those for the mouse might be expected.
Except, @Art has been refuted by experimental results which contradicts his conclusion.
Therefore, this conclusion is still valid
In the case of Polar bear, there is good theoretically well-grounded reason to think that more efficient lipid metabolism arose by degradative mutations of APOB gene .
Association between the apolipoprotein B signal peptide gene insertion/deletion polymorphism and male infertility
Peterlin, B; Zorn, B; Volk, M; Kunej, T
…In this case-control study, we searched for an association between the insertion/deletion (I/D) polymorphism of the APOB gene and male infertility in 560 Slovene Caucasian men. The study group consisted of 310 infertile patients: 115 with azoospermia and 195 with oligoasthenoteratozoospermia (OAT) and a control group of 250 fertile men. We found a statistically significant difference in the genotype distribution between the two groups (chi2 = 6.315, P = 0.043). A separate analysis of azoospermic and OAT patients demonstrated that significant differences in genotype distribution were limited to the OAT group (chi2 = 7.011, P = 0.030). The presence of the D allele (DD or ID genotypes) conferred a 1.6 risk [chi2 = 6.089, P = 0.014, 95% confidence interval (95% CI) = 1.102-2.347] for male infertility in the OAT group of patients. … These data suggest that genetic variation in the signal peptide of the APOB gene (I/D polymorphism) might be a risk factor for the development of male infertility.
Although the authors of the Slovenian study reported the association of deletion within OAT, it was marginally significant (P 5 .014; at 95% significance level, when Bonferroni correction applied: P , .05/2 5 .025). The difference between these 2 studies could very well be explained by the ethnic difference of the study populations.
On the other hand, there is no ambiguity about the mouse knockout work. Moreover, it is clear that Behe was referring to the mouse knockout work, and not to marginally relevant (when it comes to the natures and outcomes of the genetic alterations) epidemiological studies in humans that give conflicting outcomes.