"Sniegowski and colleagues have found that three of 12
independently propagated clonal populations of E. coli, which
were serially cultured over 10,000 generations and thereby
subjected to alternating periods of growth and stasis, had a
mutator phenotype which was due to defects in genes involved in
DNA repair.
"These papers transcend the assumption that mutations are
spread more or less evenly through a populations: this assumption
was only reasonable when mutation was considered to be a direct
result of random insults from outside an organism. Mutations are
now known to be due to processing of the internal consequences of
such damage, as well as to endogenous processes. The internal
procesing -a part of DNA metabolism--is carried out by gene
products whose alleles have profound effects on the generation of
variation. Alleles that predispose other genes to (possibly
beneficial) mutations may hitchike, because the mutator allele
and the phenotypically selected alleles of other genes are
linked, especially in asexual clonal populations."~E. Richard
Moxon and David S. Thaler, "The Tinkerer's Evolving Tool-box,"
Nature, 387(June 12, 1997):659-662, p. 659
The evolutionary implications of these things are explained by this:
"Take the hypothetical genome of a pathogenic bacterium,
comprising 2,000 genes including seven contingency genes (A-G),
each of which can reversibly switch at a frequency of 10-3 per
bacterium per generation. Assume that each gene is a binary
genetic switch (for example, A to A'), with corresponding
phenotypes a or a' up to g or g'. If these genes switch
independently, this gives 128 different phenotypic possibilities.
Suppose that a bacterium of phenotype a,b,c,d', e,f,g is optimal
for colonization of a host's epithelial cells, but long-term
colonization is fovourde by entry into host cells. Now suppose
that bacteria with the phenotype a',b,c,d,e,f',g'(involving four
switches from the original) are best able to invade and survive
in the cells of the host: these baceria will be selected as the
adaptive phenotype. This is a rare event--about one in a
trillion cells. But a population of cells with a 100-fold
increase in mutation rate will, on average, contain an individual
of the requisite genotype when the population size is only
10,000. This phenotypic variation, which is stochastic with
respect to the timing of switching but has a programmed genomic
location, allows a large repertoire of phenotypic solutions to be
explored, while minimizing deleterious effects on fitness."~E.
Richard Moxon and David S. Thaler, "Algorithms for Generating
Evolutionary Variation," Nature, 387(June 12, 1997):659-662, p.
661
The philosophical questions I see for the PC position are:
If God created the various life forms and evolution didn't occur, why then
did God include the ability for mutator strains to arise?
There are two sub-issues. First, since this ability helps pathogens, it
raises the problem of evil, for we have God creating a system, which can
easily mutate to a mutator strain which increases the genomic fitness of a
pathogen under certain circumstances.
Secondly, if God did not use random mutation, why would He create a system
which saves the strain from a hostile environment by use of random mutation?
Are the implications of mutator strains as I suggest? I will sit back and
listen.
Other references which should serve as entry to the literature:
Michael D. Gross and Eli
C. Siegel, "Incidence of Mutator Strains in Escherichia Coli and
Coliforms in Nature," Mutation Research 91(1981):107-110
J.E. LeClerc
et al, "High Mutation Frequencies Among Escherichia coli and
Salmonella Pathogens." Science 274 Nov. 15, 1996, p. 1208-1211,
p. 1208
Paul D. Sniegowski,
Philip J. Gerrish and Richard E. Lenski, "Evolution of High
Mutation Rates in Experimental Populations of E. coli,"
Nature,387(June 12, 1997):703-705, p. 703
glenn
Foundation, Fall and Flood
http://www.isource.net/~grmorton/dmd.htm