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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hersh, M. N.
Right arrow Articles by Rosenberg, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hersh, M. N.
Right arrow Articles by Rosenberg, S. M.

 Previous Article  |  Next Article 

Journal of Bacteriology, April 2006, p. 2336-2342, Vol. 188, No. 7
0021-9193/06/$08.00+0     doi:10.1128/JB.188.7.2336-2342.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

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,{dagger} Kimberly J. Ross,1,{ddagger} and Susan M. Rosenberg1,2*

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.

* Corresponding author. Mailing address: Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Room S809A Mail Stop BCM225, Houston, TX 77030-3411. Phone: (713) 798-6924. Fax: (713) 798-8967. E-mail: smr{at}bcm.tmc.edu.

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

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

Journal of Bacteriology, April 2006, p. 2336-2342, Vol. 188, No. 7
0021-9193/06/$08.00+0     doi:10.1128/JB.188.7.2336-2342.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Larrea, A. A., Pedroso, I. M., Malhotra, A., Myers, R. S. (2008). Identification of two conserved aspartic acid residues required for DNA digestion by a novel thermophilic Exonuclease VII in Thermotoga maritima. Nucleic Acids Res 36: 5992-6003 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»