THE ENZYME FOLD FALLACY OF DOUGLAS AXE
Meyer brought up the work of fellow I.D.ist Douglas Axe. Axe claims that new genes and/or protein folds are too improbable to evolve by random mutations and hence inaccessible to evolution:
Basically every gene, every new protein fold... there is nothing of significance that we can show [that] can be had in that gradualistic way. It’s all a mirage. None of it happens that way.
However, the evidence from Lenski’s ongoing experiment demonstrates that new genes can indeed arise as FCTs recombine, and the genomics evidence that suggests that this mechanism is widespread. If indeed new genes can be produced by recombining FCTs to create new proteins with new properties, it now falls to Axe to explain why this is not a threat to his claim that new genes/protein folds cannot be produced through evolution.
There is nothing wrong, in principle, with attempting to calculate the proportion of sequence space that will yield functional proteins/protein folds. It is just very difficult to do (e.g. How do you determine a priori whether a given protein is “functional?" And to what degrees of functionality?) and so it’s quite easy to generate numbers that are meaningless. The bottom line is that such a calculation is very difficult to make with any high degree of accuracy. Also, Axe's calculation was based on erroneous assumptions that cause it to be off by several orders of magnitude. See Arthur Hunt's evaluation of Axe's paper that Meyer cited, and thatshows where Axe went wrong.
Axe claims that the research he cites, "The Evolutionary Accessibility of New Enzymes Functions: A Case Study from the Biotin Pathway," tests an evolutionary hypothesis, i.e., by studying whether one extant enzyme in a family of enzymes could have evolved from another extant enzyme in the same family. But that is not what evolutionists propose, they propose that both evolved from a common ancestor enzyme, not from another enzyme in the same extant family. Axe and Gauger are making precisely the same error that creationists Comfort and Cameron made when they came up with their Croco-Duck argument against evolution, namely that they think "common descent" means that related modern day species evolved from each other rather than from a common ancester. That's like claiming "common descent" means that I am descended from my living cousin Keith.
Even young-earth creationist biochemist Todd Wood rebutted that particular claim more than a year ago. Wood wrote
"Instead of ancestral reconstruction, Gauger and Axe focused directly on converting an existing enzyme into another existing enzyme. That left me scratching my head, since no evolutionary biologist would propose that an extant enzyme evolved directly into another extant enzyme. So they're testing a model that no one would take seriously? Hmmm."
Axe and Gauger quite simply didn't test an evolutionary hypothesis in the paper Axe cited, but Axe continues to claim that it says something about the limits of evolution. But when even an honest young-earth creationist sees the error, persisting in it is no more than perverse. For further comments click here.
Douglas Axe also wrote Chapter 2 of Science and Human Origins by the Discovery Institute house press, in which Axe claims that unless we can identify each and every mutation between humans and our common ancestor with chimps and exactly how each arose and why they were favored, there's room for a Designer. That argument is addressed here, and here.
Those like Douglas Axe who claim it's impossible to turn a chimpanzee into Homo Sapiens via random mutations and natural selection don't seem to be aware that the common ancestor's DNA would most probably be nearer to both chimp and human DNA than either are presently to each other, because when there's a fork in the road that leads to two different destinations you have to go back to the fork in the road to study where things began to change. In fact the distance from the fork to each rival destination (chimp or human) is half as far as the distance back down one line to the fork and up the other line to the rival destination.
Does Axe consider in his calculations that there may be natural restraints concerning how things naturally interact within the cell, with some mutations being more common than others? Such natural restraints need not be due to "intelligent design," but to ways molecules and entire molecular processes interact. (Speaking of which see the book Life's Ratchet.)
Does Axe consider that the vast majority of mutations are neither deleterious nor beneficial but neutral, so we cannot predict all the possible ways neutral mutations may accumulate until something new and at least semi-functional develops?
Does Axe consider that enzymes are arranged into groups that are similar to one another, which suggests a common ancestor enzyme that underwent duplication and further minor mutations, allowing it to fit into an already ongoing process?
Can Axe predict how many or few mutations, or what types of mutations, may lead to a similar benefit There’s a wide variety of possible mutations that a single bacterium can undergo that increase its resistance to antibiotics, same with insect resistance to pesticides. Sometimes a gene is omitted, and that helps protects them, sometimes a gene is duplicated, and that helps protect them. Some mosquitoes resistant to DDT were found to have multiple copies of the esterase genes that help them detoxify it; some cotton budworms were found to no longer possess the same biochemical target that the DDT poison aims at inside the insect; and some houseflies were found to have proteins that no longer transport the poison to its target inside the insect. So there are a variety of possible mutations that can reduce the killing effects of a pesticide on an organism, and only one of those different types of mutations has to occur in order for the organism to develop some form of DDT resistance. This increases the odds that such resistance could occur via random mutations. The study of insect resistance to insecticides as well as bacterial resistance to antibiotics, as well as the human immune system's ability to produce random keys till one fits the lock of an invading microorganism (like an internal version of mutation and natural selection in action), are fascinating.
