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Journal of Bacteriology, November 2001, p. 6487-6490, Vol. 183, No. 21
Department of Molecular Microbiology and
Immunology, Keck School of Medicine, University of Southern California,
Los Angeles, California 900331, and
Department of Chemistry, Wayne State University, Detroit,
Michigan 482022
Received 19 April 2001/Accepted 27 July 2001
In Escherichia coli and related bacteria, the
very-short-patch (VSP) repair pathway uses an endonuclease, Vsr, to
correct T · G mismatches that result from the deamination of
5-methylcytosines in DNA to C · G. The products of
mutS and mutL, which are required for adenine
methylation-directed mismatch repair (MMR), enhance VSP repair.
Multicopy plasmids carrying mutS alleles that are dominant
negative for MMR were tested for their effects on VSP repair. Some
mutS mutations (class I) did not lower VSP repair in a
mutS+ background, and most class I mutations
increased VSP repair in mutS cells more than plasmids
containing mutS+. Other plasmid-borne
mutS mutations (class II) and mutS+
decreased VSP repair in the mutS+ background.
Thus, MutS protein lacking functions required for MMR can still
participate in VSP repair, and our results are consistent with a model
in which MutS binds transiently to the mispair and then translocates
away from the mispair to create a specialized structure that enhances
the binding of Vsr.
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.21.6487-6490.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Interaction of MutS and Vsr: Some Dominant-Negative
mutS Mutations That Disable Methyladenine-Directed Mismatch
Repair Are Active in Very-Short-Patch Repair
*
Corresponding author. Mailing address: 463 Chemistry
Building, Department of Chemistry, Wayne State University, Detroit, MI 48202. Phone: (313) 577-2547, Fax: (313) 577-8822. E-mail:
axb{at}chem.wayne.edu.
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