This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
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 Herzberg, K.
Right arrow Articles by Heyer, W.-D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Herzberg, K.
Right arrow Articles by Heyer, W.-D.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, November 2006, p. 8396-8409, Vol. 26, No. 22
0270-7306/06/$08.00+0     doi:10.1128/MCB.01317-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Phosphorylation of Rad55 on Serines 2, 8, and 14 Is Required for Efficient Homologous Recombination in the Recovery of Stalled Replication Forks{triangledown},{dagger}

Kristina Herzberg,1,{ddagger} Vladimir I. Bashkirov,1,{ddagger},§ Michael Rolfsmeier,1,# Edwin Haghnazari,1,¶ W. Hayes McDonald,2,|| Scott Anderson,2 Elena V. Bashkirova,1,{dagger}{dagger} John R. Yates III,2 and Wolf-Dietrich Heyer1,3*

Sections of Microbiology,1 Molecular and Cellular Biology, Center for Genetics and Development, University of California, Davis, California 95616-8665,3 Department of Cell Biology, SR-11, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 923072

Received 18 July 2006/ Returned for modification 2 August 2006/ Accepted 28 August 2006

DNA damage checkpoints coordinate the cellular response to genotoxic stress and arrest the cell cycle in response to DNA damage and replication fork stalling. Homologous recombination is a ubiquitous pathway for the repair of DNA double-stranded breaks and other checkpoint-inducing lesions. Moreover, homologous recombination is involved in postreplicative tolerance of DNA damage and the recovery of DNA replication after replication fork stalling. Here, we show that the phosphorylation on serines 2, 8, and 14 (S2,8,14) of the Rad55 protein is specifically required for survival as well as for normal growth under genome-wide genotoxic stress. Rad55 is a Rad51 paralog in Saccharomyces cerevisiae and functions in the assembly of the Rad51 filament, a central intermediate in recombinational DNA repair. Phosphorylation-defective rad55-S2,8,14A mutants display a very slow traversal of S phase under DNA-damaging conditions, which is likely due to the slower recovery of stalled replication forks or the slower repair of replication-associated DNA damage. These results suggest that Rad55-S2,8,14 phosphorylation activates recombinational repair, allowing for faster recovery after genotoxic stress.

* Corresponding author. Mailing address: Section of Microbiology, University of California, Davis, Davis, CA 95616-8665. Phone: (530) 752-3001. Fax: (530) 752-3011. E-mail: wdheyer{at}ucdavis.edu.

{triangledown} Published ahead of print on 11 September 2006.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{ddagger} These authors made equal contributions and share first authorship.

§ Present address: Applied Biosystems, Foster City, CA 94404.

# Present address: School of Molecular Biosciences, Washington State University, Pullman, WA 99163.

Present address: Scios, Inc., Fremont, CA 94555.

|| Present address: Oak Ridge National Laboratory, Oak Ridge, TN 37831.

{dagger}{dagger} Present address: Novozymes Biotech, Inc., Davis, CA 95616.

Molecular and Cellular Biology, November 2006, p. 8396-8409, Vol. 26, No. 22
0270-7306/06/$08.00+0     doi:10.1128/MCB.01317-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hashimoto, M., Taniguchi, M., Yoshino, S., Arai, S., Sato, K. (2008). S Phase-preferential Cre-recombination in Mammalian Cells Revealed by HIV-TAT-PTD-mediated Protein Transduction. J Biochem 143: 87-95 [Abstract] [Full Text]  
  • Curcio, M. J., Kenny, A. E., Moore, S., Garfinkel, D. J., Weintraub, M., Gamache, E. R., Scholes, D. T. (2007). S-Phase Checkpoint Pathways Stimulate the Mobility of the Retrovirus-Like Transposon Ty1. Mol. Cell. Biol. 27: 8874-8885 [Abstract] [Full Text]  
  • Mankouri, H. W., Ngo, H.-P., Hickson, I. D. (2007). Shu Proteins Promote the Formation of Homologous Recombination Intermediates That Are Processed by Sgs1-Rmi1-Top3. Mol. Biol. Cell 18: 4062-4073 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»