help button home button Genetics Appl Env Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Roth, J. R.
Right arrow Articles by Andersson, D. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roth, J. R.
Right arrow Articles by Andersson, D. I.
Genetics, Vol. 163, 1483-1496, April 2003, Copyright © 2003

Regulating General Mutation Rates: Examination of the Hypermutable State Model for Cairnsian Adaptive Mutation

John R. Rotha, Eric Kofoida, Frederick P. Rothb, Otto G. Bergc, Jon Segera, and Dan I. Anderssond
a Department of Biology, University of Utah, Salt Lake City, Utah 84122,
b Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115,
c Department of Molecular Evolution, Evolution Biology Centre, Uppsala University, SE-75236 Uppsala, Sweden
d Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden

Corresponding author: John R. Roth, University of California, Davis, CA 95616., jrroth{at}ucdavis.edu (E-mail)

Communicating editor: M. W. FELDMAN

In the lac adaptive mutation system of Cairns, selected mutant colonies but not unselected mutant types appear to arise from a nongrowing population of Escherichia coli. The general mutagenesis suffered by the selected mutants has been interpreted as support for the idea that E. coli possesses an evolved (and therefore beneficial) mechanism that increases the mutation rate in response to stress (the hypermutable state model, HSM). This mechanism is proposed to allow faster genetic adaptation to stressful conditions and to explain why mutations appear directed to useful sites. Analysis of the HSM reveals that it requires implausibly intense mutagenesis (105 times the unselected rate) and even then cannot account for the behavior of the Cairns system. The assumptions of the HSM predict that selected revertants will carry an average of eight deleterious null mutations and thus seem unlikely to be successful in long-term evolution. The experimentally observed 35-fold increase in the level of general mutagenesis cannot account for even one Lac+ revertant from a mutagenized subpopulation of 105 cells (the number proposed to enter the hypermutable state). We conclude that temporary general mutagenesis during stress is unlikely to provide a long-term selective advantage in this or any similar genetic system.





This article has been cited by other articles:


Home page
J. Bacteriol.Home page
R. T. Cirz, M. B. Jones, N. A. Gingles, T. D. Minogue, B. Jarrahi, S. N. Peterson, and F. E. Romesberg
Complete and SOS-Mediated Response of Staphylococcus aureus to the Antibiotic Ciprofloxacin
J. Bacteriol., January 15, 2007; 189(2): 531 - 539.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
E. Kugelberg, E. Kofoid, A. B. Reams, D. I. Andersson, and J. R. Roth
Multiple pathways of selected gene amplification during adaptive mutation
PNAS, November 14, 2006; 103(46): 17319 - 17324.
[Abstract] [Full Text] [PDF]


Home page
GeneticsHome page
M. E. Pettersson, D. I. Andersson, J. R. Roth, and O. G. Berg
The Amplification Model for Adaptive Mutation: Simulations and Analysis
Genetics, February 1, 2005; 169(2): 1105 - 1115.
[Abstract] [Full Text] [PDF]


Home page
J. Bacteriol.Home page
J. R. Roth and D. I. Andersson
Adaptive Mutation: How Growth under Selection Stimulates Lac+ Reversion by Increasing Target Copy Number
J. Bacteriol., August 1, 2004; 186(15): 4855 - 4860.
[Full Text] [PDF]


Home page
J. Bacteriol.Home page
R. Tegova, A. Tover, K. Tarassova, M. Tark, and M. Kivisaar
Involvement of Error-Prone DNA Polymerase IV in Stationary-Phase Mutagenesis in Pseudomonas putida
J. Bacteriol., May 1, 2004; 186(9): 2735 - 2744.
[Abstract] [Full Text] [PDF]


Home page
GeneticsHome page
J. Cairns and P. L. Foster
The Risk of Lethals for Hypermutating Bacteria in Stationary Phase
Genetics, December 1, 2003; 165(4): 2317 - 2318.
[Full Text] [PDF]


Home page
GeneticsHome page
J. R. Roth, E. Kofoid, F. P. Roth, O. G. Berg, J. Seger, and D. I. Andersson
Adaptive Mutation Requires No Mutagenesis--Only Growth Under Selection: A Response
Genetics, December 1, 2003; 165(4): 2319 - 2321.
[Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
E. S. Slechta, K. L. Bunny, E. Kugelberg, E. Kofoid, D. I. Andersson, and J. R. Roth
Adaptive mutation: General mutagenesis is not a programmed response to stress but results from rare coamplification of dinB with lac
PNAS, October 28, 2003; 100(22): 12847 - 12852.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2003 by the Genetics Society of America.