At 11:15 PM 7/15/98 -0600, Bill Payne wrote:
>Glenn R. Morton wrote:
>
>> Bill, exactly why is antibiotic resistance not beneficial to a bacterium?
>
>Antibotic resistance is not a mutation, as is commonly assumed by many.
>
>"What about trying for four related mutations? 10^28. All of a sudden
>the earth isn't big enough to hold enough organisms to make that very
>likely. And we're only talking about four mutations. It would take many
>more than that to change a fish into a philosopher, or even a fish into
>a frog.
>
What you may not be aware of is that many bacteria when stressed, become
mutator strains. Dawkins writes:
"There are, indeed, genes whose effect is to control the mutation rate in
other genes. In theory one might argue that these 'mutator genes' could be
triggered by stress, and such a tendency could be favoured by some sort of
high-level natural selection. But alas, this theory turns out to have no
more support than our previous theory of beneficently directed mutation.
First, there is no evidence for it." ~ Richard Dawkins, Climbing Mount
Improbable, (New York: W. W. Norton 1996), p. 83
Consider this info.
"A mutator phenotype should be to the pathogen's advantage, affording
strategies (mutation and recombination) that permit rapid variation in an
unstable environment in order, for example, to escape immune surveillance
or elude therapeutic intervention (antibiotic resistance). The ability to
generate a large number of mutations for adaptation in a changing
environment; the opportunity to establish and propagate in the new niche of
its host; the increased potential for gene acquisition; and the requisite
linkage of the mutator phenotype, in the absence of recombination, to any
beneficial phenotype spur selection of a mutator. In contrast, placed in a
static environment, the same bacterium might be destined for extinction
(that is, mutations in vital genes are lethal), although induction of
suppressor mutations can quiet the mutator activity and attenuate this
outcome."
"It would seem that the ultimate pathogen would possess an elevated
mutation rate that is transient (or conditional), providing genetic
variation during the first few hours when the pathogen must survive,
invade, and colonize its host."J.E. LeClerc et al, "High Mutation
Frequencies Among Escherichia coli and Salmonella Pathogens." Science 274
Nov. 15, 1996, p. 1208-1211, p. 1210
"In certain mutator phenotypes, namely those deficient in methyl-directed
mismatch repair (MMR), these forces converge to increase the rate of
genetic variation. MMR is a postreplicative repair system that corrects
errors on newly synthesized DNA strands to ensure the precision of
chromosome replication. MMR is also a major barrier to interspecies gene
exchange. Consequently, bacteria defective in MMR show both an enhanced
rate of mutation (a hypermutable phenotype) and an increase in
recombination of divereges sequences; that is, they are more promiscuous.
It therefore becomes relevant to the problem of emerging pathogens to
determine the frequency of such mutator phenotypes among human pathogens."
~ J. Eugene LeClerc et al, "High Mutation Frequencies Among Escherichia
coli and Salmonella Pathogens," Science, 274(Nov. 15, 1996):1208-1211, p. 1208
**
mutator strains
"The incidence of hypermutable mutants among pathogenic strains (>1%) is
alarmingly high considering that, at equilibrium, the frequency of
deleterious alleles within a population is expected to be 10-5 to 10-3.
Our results, hoever, were partially presaged by chemostat competition
analyses." ~ J. Eugene LeClerc et al, "High Mutation Frequencies Among
Escherichia coli and Salmonella Pathogens," Science, 274(Nov. 15,
1996):1208-1211, p. 1209
**
mutator strains
"A mutator locus in E. coli K-12 (1) increases the spontaneous mutation
rate of a number of loci including that of streptomycin resistance.
Mutation rate at a p-aminobenzoic acid locus (2), a locus conferring
resistance to the phage T2(1) and a cystein locus (3) does not appear to be
affected. The auxotrophic mutation rate of the highly mutative 'Harvard
strain' of E. coli (4) seems to involve single genes. The diversity of
single requirements suggests that the genetic instability of this strain is
not confined to the vicinity of any single gene locus.
"Action of mutator genes have also been described in Drosophila, Maize,
Yeast and streptomyces. At least the mutator gene of maize seems to cause
instability of one single gene locus. This locus is not located in the
same chromosome as is the mutator gene. It is the purpose of the present
work to find how often we may expect to find strains of E. coli with high
mutation rate to streptomycin resistance. Through the study of auxotrophs
we will try to compare the genetic instabilities of such strains." ~ K.
Jyssum, "Observations on Two Types of Genetic Instability in Escherichia
Coli," Acta Pathol. Microbial. Immunol. Scand. 48:113-120, p. 113
"We found mutator strains in natural populations at a frequency of 1/408
(0.24%)"Michael D. Gross and Eli C. Siegel, "Incidence of Mutator Strains
in Escherichia coli and Coliforms in Nature," Mutation Research,
91(1981):107-110, p. 109
See also: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
>It was at this level (just four related mutations) that microbiologists
>gave up on the idea that mutations could explain why some bacteria were
>resistant to four different antibiotics at the same time.
Biologists haven't given up. Of course, given your epistemology, the
majority of biologists are flat wrong and only the outlier positions are
correct.
>> And the sickle cell gene gives some protection from malaria if it is
>> heterozygous. Are you saying that it is better for more people to die from
>> Malaria than for fewer people (the homozyous) to die from sickle cell
>> anemia? If it saves lives in a malaria infested environment, exactly why is
>> it not beneficial?
>
>Sickle cell anemia is a disease which kills 25% of the children of
>carriers of sickle cells. The sickle cell disease does protect from
>another disease, marlaria, in 50% of the sickle cell population. If you
>want to claim that the sickle cell disease is a beneficial mutation,
>I'll grant you that one, Glenn, but I tend to think of both diseases as
>part of the curse from the Garden of Eden. You appear to be in a bit of
>an awkward position, using a degenerating disease to support
>macroevolution. Your theory points up, but your data points down.
In non-malarial areas, the incidence of sickle cell are decreasing because
they are selected out of the population. But in malaria infested areas, it
remains at constant levels and indeed the Nigerian variety of sickle cell
has become predominant in malarial areas of Portugal over the past 400
years. Why? Because the Benin type of sickle cell was beneficial to the
population of Portugal and protected them from malaria.
"These patients had clinical and haematological features similar to
patients of African origin, although their growth and sexual development
appeared to be normal. The analysis of an array of polymorphic restriction
sites within the [beta]s globin gene cluster ([beta]s haplotype) showed
patterns that are known to occur in Africa. The frequencies of the three
main African [beta] s haplotypes termed Senegal, Bantu, and Benin reflect
the extent of Portuguese naval explorations. It is concluded that the
sickle cell gene in Portugal has probably been imported from Africa and has
been amplified in comparison with other genes characteristic for African
races because of the selective advantage of AS heterozygotes in an area
endemic for malaria." ~ C. Monteiro et al, "The Frequency and Origin of the
Sickle cell mutation in the District of Coruche/Portugal," Human Genetics,
82(1989):255-258, p. 255
glenn
Adam, Apes and Anthropology
Foundation, Fall and Flood
& lots of creation/evolution information
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