Joel Duff (crinoid@midwest.net)
Wed, 28 Apr 1999 08:37:13 -0500

I recently heard James Shapiro talk again on the topic of "What will we
think about evolution in the 21st century." Once again he expounded on
the idea that random mututions are not enough to produce a diverse genetic
pool of varients from which evolution (ie selection) could draw upon to
create a gradualistic evolutionary pattern. Rather he argued from several
examples that the capacity for evolution is the product of evolution itself
(evolvibility) thus explaining why some organisms evolve at different rates
and why so many different patterns of evolution are seen today and in the
fossil record. One thing that this hinges upon is the idea that organisms
can effectively control their own mutation rates increasing them at times
when they are needed. Just in the last few years the more and more
examples of organisms that effectly can specific target genes or gene
systems with various types of mutations based on environmental cues have
been found. Personally I think that we are only at the tip of the iceberg
in terms of understanding the ways in which organisms can effectly shuffle
and change their own genomes. What made me think of this today is that
that I just say in the most recent PNAS yet another example demonstrating
mutation rate changes due to environmental stress in E. coli.

Joel Duff

Abstract below:

Vol. 96, Issue 9, 5089-5094, April 27, 1999
Hypermutation in derepressed operons of Escherichia coli K12

(stringent response / transcription / mutations)

Barbara E. Wright*, Angelika Longacre, and Jacqueline M. Reimers

Division of Biological Sciences, University of Montana, Missoula, MT 59812

Communicated by E. R. Stadtman, National Heart, Lung and Blood Institute,
Bethesda, MD, February 16, 1999 (received for review December
15, 1998)

This article presents evidence that starvation for leucine in an
Escherichia coli auxotroph triggers metabolic activities that specifically
target the leu operon
for derepression, increased rates of transcription, and mutation.
Derepression of the leu operon was a prerequisite for its activation by the
signal nucleotide,
guanosine tetraphosphate, which accumulates in response to nutritional
stress (the stringent response). A quantitative correlation was established
leuB mRNA abundance and leuB reversion rates. To further demonstrate that
derepression increased mutation rates, the chromosomal leu operon was
placed under the control of the inducible tac promoter. When the leu operon
was induced by isopropyl-D-thiogalactoside, both leuB mRNA abundance and
leuB reversion rates increased. These investigations suggest that guanosine
tetraphosphate may contribute as much as attenuation in regulating leu
expression and that higher rates of mutation are specifically associated
with the derepressed leu operon.