YOU refuted Shapiro by providing citations to papers Shapiro relied on for his claims - papers written by people that later OVERTURNED their original conclusions by performing more expansive research. Just as I documented. That you reject this obvious undercutting of your new hero's claims is your usual thing - you've done the same with Haldane, Sanford, etc. It is your calling-card, of a sort. Once you realize you've lost on one issue, you not-so-cleverly just move on to another, hoping your 'new' hero (whom you misunderstand and misrepresent) can help you do what your other heroes did not.
I copy-paste below your abject
failure:
...did you not see the dates of your citations?
2002 and 2007.
To be clear, you presented those 2 papers supposedly to counter my statement:
"No. That has not been established. Mutations - and this includes the insertions of mobile elements - occur WITHOUT the 'needs' of the organism playing a role. This was established in many research publications, one of which I cited earlier and was written by one of Cairns' (whose group published among the first papers claiming to have identified nonrandom mutations positively affecting fitness) associates."
To be clearer, the paper I had cited earlier - by one of Cairns' collaborators and whom Shapiro had cited himself - indicates (2004):
"Fairly early on in our studies, Cairns and I eliminated the hypothesis that mutations were “directed” toward a useful goal. The first negative evidence was obtained not with FC40, but with SM195. SM195 has an amber mutation in lacZ and so reverts both by intragenic mutations and by the creation of tRNA suppressors (11). The continued appearance of extragenic suppressors during lactose selection allowed us to dismiss the hypothesis that the selective conditions “instructed” the cell to make appropriate mutations—in the case of extragenic suppressors, there is no direct path from the phenotype (Lac+) to the mutated gene (encoding a tRNA) (23). Later it was shown that about two-thirds of the late-appearing Lac+ revertants of SM195 were due to slow-growing ochre suppressors that probably arose during growth prior to lactose selection (57). Nonetheless, the continued appearance of fast-growing amber suppressors in addition to the true revertants demonstrated that mutations appear elsewhere than in the gene directly under selection (24)."
Yet again, you cite a review article by Shapiro, one in which, as seems to be his norm, he simply combs the literature for things he thinks supports his cause. I do note that he did not cite the 2004 Foster paper. Interesting.
Another from Foster (2012):
EcoSal Plus .
2012 Nov;5(1):10.1128/ecosalplus.7.2.3. doi: 10.1128/ecosalplus.7.2.3.
Stress-Induced Mutagenesis
Ashley B Williams, Patricia L Foster
PMID: 26442828 PMCID: PMC423720
"...recent results from a variety of experimental systems suggest that mutation rates can increase in response to selective pressures. This chapter summarizes data demonstrating that, under stressful conditions, Escherichia coli and Salmonella can increase the likelihood of beneficial mutations by modulating their potential for genetic change.[NOTE - do NOT assume that this means that this paper supports the NGE crud or that it supports 'directed mutation' - indeed, they explain (see below quote) that the increased beneficial mutations are the result of overall hypermutation] Several experimental systems used to study stress-induced mutagenesis are discussed, with special emphasis on the Foster-Cairns system for "adaptive mutation" in E. coli and Salmonella. Examples from other model systems are given to illustrate that stress-induced mutagenesis is a natural and general phenomenon that is not confined to enteric bacteria. Finally, some of the controversy in the field of stress-induced mutagenesis is summarized and discussed, and a perspective on the current state of the field is provided."
and:
"During lactose selection Lac- cells accumulate non-selected mutations, disproving the hypothesis that mutations to Lac+ are “directed” by the selective pressure (41, 76, 77, 183). The rate of accumulation of non-selected mutations is higher on the episome than on the chromosome (41, 76, 77), possibly due to more frequent episomal replication and recombination. "
Also of note is the brief discussion of the fact that the 'beneficial mutations' that occur in their model system occur spontaneously, and that in the hypermutation state, they increase by an order of magnitude (from 10^9 to 10^8), which sounds like a lot, but then, it happens a lot anyway.
Can't get much clearer than that. But you keep pretending that you've scored points for your IDC fantasies. Everyone else will see the facts.
