DinB upregulation is the sole role of the SOS response in stress-induced mutagenesis in Escherichia coli

Rodrigo S. Galhardo, Robert Do, Masami Yamada, Errol C. Friedberg, P. J. Hastings, Takehiko Nohmi, Susan M. Rosenberg

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

Stress-induced mutagenesis is a collection of mechanisms observed in bacterial, yeast, and human cells in which adverse conditions provoke mutagenesis, often under the control of stress responses. Control of mutagenesis by stress responses may accelerate evolution specifically when cells are maladapted to their environments, i.e., are stressed. It is therefore important to understand how stress responses increase mutagenesis. In the Escherichia coli Lac assay, stress-induced point mutagenesis requires induction of at least two stress responses: the RpoS-controlled general/starvation stress response and the SOS DNAdamage response, both of which upregulate DinB error-prone DNA polymerase, among other genes required for Lac mutagenesis. We show that upregulation of DinB is the only aspect of the SOS response needed for stress-induced mutagenesis. We constructed two dinB(oc) (operator-constitutive) mutants. Both produce SOS-induced levels of DinB constitutively. We find that both dinB(oc) alleles fully suppress the phenotype of constitutively SOS-"off" lexA(Ind-) mutant cells, restoring normal levels of stress-induced mutagenesis. Thus, dinB is the only SOS gene required at induced levels for stress-induced point mutagenesis. Furthermore, although spontaneous SOS induction has been observed to occur in only a small fraction of cells, upregulation of dinB by the dinB(oc) alleles in all cells does not promote a further increase in mutagenesis, implying that SOS induction of DinB, although necessary, is insufficient to differentiate cells into a hypermutable condition.

Original languageEnglish (US)
Pages (from-to)55-68
Number of pages14
JournalGenetics
Volume182
Issue number1
DOIs
StatePublished - May 1 2009

ASJC Scopus subject areas

  • Genetics

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