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

J. Biol. Chem., Vol. 278, Issue 48, 48485-48490, November 28, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/48/48485    most recent M304217200v1 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Shea, M. E. Articles by Hiasa, H. Search for Related Content PubMed PubMed Citation Articles by Shea, M. E. Articles by Hiasa, H. Social Bookmarking                      What's this?

The RuvAB Branch Migration Complex Can Displace Topoisomerase IV·Quinolone·DNA Ternary Complexes^*

Molly E. Shea and Hiroshi Hiasa

From the Department of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota 55455

Quinolone antimicrobial drugs target both DNA gyrase and topoisomerase IV (Topo IV) and convert these essential enzymes into cellular poisons. Topoisomerase poisoning results in the inhibition of DNA replication and the generation of double-strand breaks. Double-strand breaks are repaired by homologous recombination. Here, we have investigated the interaction between the RuvAB branch migration complex and the Topo IV·quinolone·DNA ternary complex. A strand-displacement assay is employed to assess the helicase activity of the RuvAB complex in vitro. RuvAB-catalyzed strand displacement requires both RuvA and RuvB proteins, and it is stimulated by a 3'-non-hybridized tail. Interestingly, Topo IV·quinolone·DNA ternary complexes do not inhibit the translocation of the RuvAB complex. In fact, Topo IV·quinolone·DNA ternary complexes are reversed and displaced from the DNA upon their collisions with the RuvAB complex. These results suggest that the RuvAB branch migration complex can actively remove quinolone-induced covalent topoisomerase·DNA complexes from DNA and complete the homologous recombination process in vivo.

Received for publication, April 22, 2003 , and in revised form, September 2, 2003.

^* This work was supported by grants from the National Institutes of Health (GM59465), the University of Minnesota Graduate School Grant-in-Aid Program, and the Minnesota Medical Foundation. 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.

To whom correspondence should be addressed: 6-120 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455. Tel.: 612-626-3101; Fax: 612-625-8408; E-mail: hiasa001{at}tc.umn.edu.

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

This article has been cited by other articles:

				J. Kang and M. J. Blaser Repair and Antirepair DNA Helicases in Helicobacter pylori J. Bacteriol., June 15, 2008; 190(12): 4218 - 4224. [Abstract] [Full Text] [PDF]

				K. Drlica, M. Malik, R. J. Kerns, and X. Zhao Quinolone-Mediated Bacterial Death Antimicrob. Agents Chemother., February 1, 2008; 52(2): 385 - 392. [Full Text] [PDF]