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Single-Strand-Specific Exonucleases Prevent Frameshift Mutagenesis by Suppressing SOS Induction and the Action of DinB/DNA Polymerase IV in Growing Cells

Megan N. Hersh,¹ Liza D. Morales,^1, Kimberly J. Ross,^1, and Susan M. Rosenberg^1,2*

Departments of Molecular and Human Genetics,¹ Biochemistry and Molecular Biology and Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Room S809A Mail Stop BCM225, Houston, Texas 77030-3411²

Received 5 October 2005/ Accepted 11 January 2006

Escherichia coli strains carrying null alleles of genes encoding single-strand-specific exonucleases ExoI and ExoVII display elevated frameshift mutation rates but not base substitution mutation rates. We characterized increased spontaneous frameshift mutation in ExoI^– ExoVII^– cells and report that some of this effect requires RecA, an inducible SOS DNA damage response, and the low-fidelity, SOS-induced DNA polymerase DinB/PolIV, which makes frameshift mutations preferentially. We also find that SOS is induced in ExoI^– ExoVII^– cells. The data imply a role for the single-stranded exonucleases in guarding the genome against mutagenesis by removing excess single-stranded DNA that, if left, leads to SOS induction and PolIV-dependent mutagenesis. Previous results implicated PolIV in E. coli mutagenesis specifically during starvation or antibiotic stresses. Our data imply that PolIV can also promote mutation in growing cells under genome stress due to excess single-stranded DNA.

Present address: Thrombosis Research Section, Department of Medicine, Baylor College of Medicine, Houston, TX 77030.

Present address: 331 E. Cleveland St., Coopersville, MI 49404.