HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 283, Issue 21, 14198-14204, May 23, 2008

This Article Full Text Full Text (PDF) All Versions of this Article: 283/21/14198    most recent M801511200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Baitin, D. M. Articles by Cox, M. M. Search for Related Content PubMed PubMed Citation Articles by Baitin, D. M. Articles by Cox, M. M. Social Bookmarking                      What's this?

SSB Antagonizes RecX-RecA Interaction^*

From the Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706-1544

The RecX protein of Escherichia coli inhibits the extension of RecA protein filaments on DNA, presumably by binding to and blocking the growing filament end. The direct binding of RecX protein to single-stranded DNA is weak, and previous reports suggested that direct binding to DNA did not explain the effects of RecX. We now demonstrate that elevated concentrations of SSB greatly moderate the effects of RecX protein. High concentrations of the yeast RPA protein have the same effect, suggesting that the effect is not species-specific or even specific to bacterial SSB proteins. A direct SSB-RecX interaction is thus unlikely. We suggest that SSB is blocking access to single-stranded DNA. The evident competition between RecX and SSB implies that the mechanism of RecX action may involve RecX binding to both RecA protein and to DNA. We speculate that the interaction of RecX protein and RecA may enable an enhanced DNA binding by RecX protein. The effects of SSB are increased if the SSB C terminus is removed.

Received for publication, February 25, 2008 , and in revised form, April 1, 2008.

^* This work was supported, in whole or in part, by National Institutes of Health Grant GM32335 (to M. M. C.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Biochemistry, University of Wisconsin-Madison, 433 Babcock Dr., Madison, WI 53706-1544. Tel.: 608-262-1181; Fax: 608-265-2603; E-mail: cox{at}biochem.wisc.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?