Expecting that engineers want their designs to be robust and able to overcome the challenges of the environment isn’t an ad hoc expectation. It flows naturally from what we could term “good design” principles.
But let’s see what this teleological perspective leads us to expect. Remember, I’m only suggesting that the original population of cells was designed. That means that if a particular structure found in extant life was designed, it would have been present in an ur-state in the first cells, from which it has diversified and become modified by evolution. For example, antifreeze proteins that evolved in the Antarctic notothenioids 10-14 million years ago would be a poor candidate for design.
This means that I would expect the phylogenetic distribution of the machinery required for regulated mutagenesis, such as the SOS response, to show that the system traces back to an ur-state in the first bacteria. And indeed, both recA and lexA, which play key roles in the regulation of the SOS response, are practically universal in bacteria. And those bacterial groups which lack them are thought to have secondarily lost them. This points to the existence of an original SOS response core, which evolution has then unfolded into the systems we see today.
Distribution of the lexA gene across the bacterial domain, based on the phylogenetic distribution derived from RecA protein sequences (Eisen,1995). Light grey areas enclose phylogenetic groups and dark grey areas indicate the presence of lexA . Filled circles denote species that have undergone substantial genomic reduction. From Erill, Campoy & Barbé, 2007
This expectation of an ur-state stands in sharp contrast to the expectations of the ateleological view, in which every organism with structure X is descended from an organism without that structure, all the way back to the first replicator.
Scientists estimate that Earth has about one trillion microbial species, with 98 percent yet to be discovered. In other words, there are lots of opportunities for discoveries of bacteria that represent this supposed pre-SOS response state, dashing my teleological expectatins.
One final note: I don’t have a theory. I have a conjecture, which I’m trying to flesh out in my spare time.
The title of the review? I linked to the review and told people of its title. The title of my own post “PLOS Genetics on non-random mutations” focused on what I found interesting about the article, and I wrote nothing about whether or not I thought regulated mutagenesis was consistent with some interpretation of the Modern Synthesis.
It really says something about the hair trigger that some ID critics seem to have that merely mentioning the title of a review one is discussing opens one up to accusations that one is misrepresenting the contents of the review.
I suppose one could in principle equip cells with a sort of molecular computer which could analyse new challenges, predict the protein that would be required to face the challenge and which mutations would result in that protein, and induce the desired mutation. But I think the resources required to maintain such a computer would be more taxing on the cell that any benefit gained from it.
A better solution, in my view, is to make life itself the computer. Have lots of cells experiment with solving a problem and let the succesful attempts spread by “cross-talk” between cells, i.e. horizontal genetic transfer and exchange of plasmids.