Bruce Levin and colleagues collected E. coli from the diapers of infants at
a day-care center. 25% of the bacteria were streptomycin resistant forms
carrying the rpsL mutation for streptomycin resistance. Bacteria carrying
this gene are weaker than the normal wild-type bacteria. This was observed
as long ago as 1955 when researchers found that 60% of the streptomycin
resistant strains could not live without streptomycin! (Theodosius
Dobzhansky, Evolution, Genetics and Man, (New York: John Wiley and Sons,
Inc., 1955), p. 98.)
However, the 25% streptomycin resistance was surprising because over the
past 30 years doctors have rarely used streptomycin. This represents 60,000
generations. So the question is what happened?
Levin et al, took some of the resistant E. coli and grew them for 160
generations in a streptomycin free culture and then let them compete
against the drug sensitive strains. The expectation from Dobzhansky's
point is that the wild types would kill the resistant strains. But, the
wild types lost! The drug resistant strains were MORE fit than the wild types.
Levin et al then took the drug resistant strains and genetically altered
the rpsL gene to be a drug sensitive. In other words, they turned the drug
resistant strains into drug sensitive strains and then they repeated the
competition. This time the formerly drug resistant strains LOST. They were
less fit. What happened?
A second mutation that overcame the deficiency in drug dependance is what
happened. The first mutation, the one for drug resistance, by itself is
harmful. The second mutation, that overcomes the deficiencey, by itself is
harmful. But together, these TWO mutations make for a better, stronger,
more resiliant bug. Together, the mutations make for a beneficial pair of
mutations.
This is what anti-evolutionists really don't understand about mutations,
they work in concert with other mutations to benefit the organism.
Science Magazine says:
"The interaction between the two mutations would acat as a kind of
ratchet, preventing bacteria from reverting to sensitivity. 'The
compensatory mutations establish an 'adaptive valley' that virturally
precludes that population of resistant bacteria from returning to drug
sensitivity,' explains Levin. And that explains why the bacteria in
Lenski's lab and possibly those in the children's diapers have not lost
their resistance. 'Those that revert, that make that one change, are at a
disadvantage,' explains Levin. The team is now trying to identify the gene
tthatcarries this compensatory mutation."
"Levin suspects that the same kind of compensatory mtuations 'will almost
certainly be found in other resistant bacteria.' But already, the findings
have 'clear, practical-and rather frightening-implications,' says Marlene
Zuk, an evolutionary biologist at the University of California, Riverside.
'It's not enough to stop using antibiotics; the bacteria aren't going to
revert to what they were before'-and antibiotics that have lost their
effectiveness won't become powerful weapons again."
~ Virginia Morell, "Antibiotic Resistance: Road of No Return," Science,
278(1997):575-576,
glenn
Adam, Apes and Anthropology
Foundation, Fall and Flood
& lots of creation/evolution information
http://www.isource.net/~grmorton/dmd.htm