MCB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 Malkova, A.
Right arrow Articles by Haber, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Malkova, A.
Right arrow Articles by Haber, J. E.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, February 2005, p. 933-944, Vol. 25, No. 3
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.3.933-944.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

RAD51-Dependent Break-Induced Replication Differs in Kinetics and Checkpoint Responses from RAD51-Mediated Gene Conversion

Anna Malkova ,{dagger},{ddagger} Maria L. Naylor,{dagger},§ Miyuki Yamaguchi,{dagger} Grzegorz Ira, and James E. Haber*

Department of Biology and Rosenstiel Center, Brandeis University, Waltham, Massachusetts

Received 13 August 2004/ Returned for modification 22 September 2004/ Accepted 25 October 2004

Diploid Saccharomyces cells experiencing a double-strand break (DSB) on one homologous chromosome repair the break by RAD51-mediated gene conversion >98% of the time. However, when extensive homologous sequences are restricted to one side of the DSB, repair can occur by both RAD51-dependent and RAD51-independent break-induced replication (BIR) mechanisms. Here we characterize the kinetics and checkpoint dependence of RAD51-dependent BIR when the DSB is created within a chromosome. Gene conversion products appear within 2 h, and there is little, if any, induction of the DNA damage checkpoint; however, RAD51-dependent BIR occurs with a further delay of 2 to 4 h and cells arrest in response to the G2/M DNA damage checkpoint. RAD51-dependent BIR does not require special facilitating sequences that are required for a less efficient RAD51-independent process. RAD51-dependent BIR occurs efficiently in G2-arrested cells. Once repair is initiated, the rate of repair replication during BIR is comparable to that of normal DNA replication, as copying of >100 kb is completed less than 30 min after repair DNA synthesis is detected close to the DSB.

* Corresponding author. Mailing address: Rosenstiel Center, Brandeis University, 415 South St., Mail Stop 029, Waltham, MA 02454-9110. Phone: (781) 736-2462. Fax: (781) 736-2405. E-mail: haber{at}brandeis.edu.

{dagger} A.M., M.L.N., and M.Y. contributed equally to this work.

{ddagger} Present address: Biology Department, Indiana University—Purdue University Indianapolis, Indianapolis, IN 46202.

§ Present address: Department of Genetics, Harvard Medical School, Boston, MA 02115.

Molecular and Cellular Biology, February 2005, p. 933-944, Vol. 25, No. 3
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.3.933-944.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2005 by the American Society for Microbiology. All rights reserved.