Abstract
Several bacterial systems show behavior interpreted as evidence for stress-induced mutagenesis (adaptive mutation), a postulated process by which nongrowing cells temporarily increase their general mutation rate. Theoretical considerations suggest that periodic stress-induced general mutagenesis would not be advantageous in the long term, due to the high cost of deleterious mutations. Alternative explanations have been tested for very few of the systems used as evidence for stress-induced mutation. In one prominent system, mutants resistant to rifampicin (RifR; rpoB; RNA polymerase) accumulate in cell populations that "age" on solid medium with little net growth. Mutant accumulation was initially attributed to stress-induced general mutagenesis in nongrowing cells. Evidence is presented that these Rif R mutants accumulate because they grow faster than parent cells during the aging period. Direct tests revealed no increase in the frequency of other mutant types during the aging period.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 11863-11868 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 105 |
| Issue number | 33 |
| DOIs | |
| State | Published - Aug 19 2008 |
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ASJC Scopus subject areas
- Genetics
- General
Cite this
Accumulation of mutants in "aging" bacterial colonies is due to growth under selection, not stress-induced mutagenesis. / Wrande, Marie; Roth, John R.; Hughes, Diarmaid.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 105, No. 33, 19.08.2008, p. 11863-11868.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Accumulation of mutants in "aging" bacterial colonies is due to growth under selection, not stress-induced mutagenesis
AU - Wrande, Marie
AU - Roth, John R.
AU - Hughes, Diarmaid
PY - 2008/8/19
Y1 - 2008/8/19
N2 - Several bacterial systems show behavior interpreted as evidence for stress-induced mutagenesis (adaptive mutation), a postulated process by which nongrowing cells temporarily increase their general mutation rate. Theoretical considerations suggest that periodic stress-induced general mutagenesis would not be advantageous in the long term, due to the high cost of deleterious mutations. Alternative explanations have been tested for very few of the systems used as evidence for stress-induced mutation. In one prominent system, mutants resistant to rifampicin (RifR; rpoB; RNA polymerase) accumulate in cell populations that "age" on solid medium with little net growth. Mutant accumulation was initially attributed to stress-induced general mutagenesis in nongrowing cells. Evidence is presented that these Rif R mutants accumulate because they grow faster than parent cells during the aging period. Direct tests revealed no increase in the frequency of other mutant types during the aging period.
AB - Several bacterial systems show behavior interpreted as evidence for stress-induced mutagenesis (adaptive mutation), a postulated process by which nongrowing cells temporarily increase their general mutation rate. Theoretical considerations suggest that periodic stress-induced general mutagenesis would not be advantageous in the long term, due to the high cost of deleterious mutations. Alternative explanations have been tested for very few of the systems used as evidence for stress-induced mutation. In one prominent system, mutants resistant to rifampicin (RifR; rpoB; RNA polymerase) accumulate in cell populations that "age" on solid medium with little net growth. Mutant accumulation was initially attributed to stress-induced general mutagenesis in nongrowing cells. Evidence is presented that these Rif R mutants accumulate because they grow faster than parent cells during the aging period. Direct tests revealed no increase in the frequency of other mutant types during the aging period.
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UR - http://www.scopus.com/inward/citedby.url?scp=50149112177&partnerID=8YFLogxK
U2 - 10.1073/pnas.0804739105
DO - 10.1073/pnas.0804739105
M3 - Article
C2 - 18701713
AN - SCOPUS:50149112177
VL - 105
SP - 11863
EP - 11868
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 33
ER -