The SOS response regulates adaptive mutation

Gregory J. McKenzie, Reuben S. Harris, Peter L. Lee, Susan M. Rosenberg

Research output: Contribution to journalArticlepeer-review

176 Scopus citations

Abstract

Upon starvation some Escherichia coli cells undergo a transient, genome- wide hypermutation (called adaptive mutation) that is recombination-dependent and appears to be a response to a stressful environment. Adaptive mutation may reflect an inducible mechanism that generates genetic variability in times of stress. Previously, however, the regulatory components and signal transduction pathways controlling adaptive mutation were unknown. Here we show that adaptive mutation is regulated by the SOS response, a complex, graded response to DNA damage that includes induction of gene products blocking cell division and promoting mutation, recombination, and DNA repair. We find that SOS-induced levels of proteins other than RecA are needed for adaptive mutation. We report a requirement of RecF for efficient adaptive mutation and provide evidence that the role of RecF in mutation is to allow SOS induction. We also report the discovery of an SOS-controlled inhibitor of adaptive mutation, PsiB. These results indicate that adaptive mutation is a tightly regulated response, controlled both positively and negatively by the SOS system.

Original languageEnglish (US)
Pages (from-to)6646-6651
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume97
Issue number12
DOIs
StatePublished - Jun 6 2000

Keywords

  • DNA repair
  • Escherichia coli
  • RecA
  • RecF
  • Signal transduction

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