This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ozgenc, A. I. Articles by Lawrence, C. W. Search for Related Content PubMed PubMed Citation Articles by Ozgenc, A. I. Articles by Lawrence, C. W.

In Vivo Evidence for a recA-Independent Recombination Process in Escherichia coli That Permits Completion of Replication of DNA Containing UV Damage in Both Strands

Ali I. Ozgenc, Edward S. Szekeres, and Christopher W. Lawrence^*

Department of Biochemistry & Biophysics, University of Rochester School of Medicine & Dentistry, Rochester, New York

Received 21 October 2004/ Accepted 13 December 2004

We have investigated recombination mechanisms promoting the completion of replication in the face of unrepaired DNA damage by transforming an isogenic set of uvrA6 excision-defective Escherichia coli strains with pUC-based plasmids in which each strand carried, at staggered positions, a single thymine-thymine pyrimidine (6-4) pyrimidinone lesion. The distance between the lesions was 28 or 8 bp in one orientation relative to the unidirectional ColE1 origin of replication or, in the other orientation, 30 or 10 bp. C-C mismatches placed opposite each of the T-T photoproducts permit unambiguous detection of the three events that can lead to the completion of replication: sister-strand recombination, translesion replication (TR) on the leading strand, and TR on the lagging strand. We find that E. coli possesses a largely constitutive, recA-independent sister-strand recombination mechanism that allows 9% or more of these severely compromised plasmids to be fully replicated. In one orientation, such recombination depends partly on recG and priA but not on ruvA, ruvB, ruvC, or mutS and is largely independent of recF. In the other orientation, recombination is dependent on none of the genes. The strains used did not contain the cryptic phage encoding recET, which encodes enzymes that promote interplasmid recombination. The nature of the recA-independent recombination mechanism is not known but could perhaps result from a template-strand-switching, or copy choice, process.

Present address: Department of Pathology, University of Washington, Seattle, WA 98195.

Present address: CuraGen Corporation, Branford, CT 06405.

This article has been cited by other articles:

• Zhang, H., Gibbs, P. E. M., Lawrence, C. W. (2006). The Saccharomyces cerevisiae rev6-1 Mutation, Which Inhibits Both the Lesion Bypass and the Recombination Mode of DNA Damage Tolerance, Is an Allele of POL30, Encoding Proliferating Cell Nuclear Antigen. Genetics 173: 1983-1989 [Abstract] [Full Text]  
• Roux, C. M., Booth, N. J., Bellaire, B. H., Gee, J. M., Roop, R. M. II, Kovach, M. E., Tsolis, R. M., Elzer, P. H., Ennis, D. G. (2006). RecA and RadA Proteins of Brucella abortus Do Not Perform Overlapping Protective DNA Repair Functions following Oxidative Burst.. J. Bacteriol. 188: 5187-5195 [Abstract] [Full Text]  
• Zhang, H., Lawrence, C. W. (2005). The error-free component of the RAD6/RAD18 DNA damage tolerance pathway of budding yeast employs sister-strand recombination. Proc. Natl. Acad. Sci. USA 102: 15954-15959 [Abstract] [Full Text]