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Molecular and Cellular Biology, November 2006, p. 8075-8086, Vol. 26, No. 21
0270-7306/06/$08.00+0     doi:10.1128/MCB.01235-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Differential Regulation of Short- and Long-Tract Gene Conversion between Sister Chromatids by Rad51C{triangledown}

Ganesh Nagaraju, Shobu Odate, Anyong Xie, and Ralph Scully*

Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215

Received 7 July 2006/ Returned for modification 2 August 2006/ Accepted 23 August 2006

The Rad51 paralog Rad51C has been implicated in the control of homologous recombination. To study the role of Rad51C in vivo in mammalian cells, we analyzed short-tract and long-tract gene conversion between sister chromatids in hamster Rad51C–/– CL-V4B cells in response to a site-specific chromosomal double-strand break. Gene conversion was inefficient in these cells and was specifically restored by expression of wild-type Rad51C. Surprisingly, gene conversions in CL-V4B cells were biased in favor of long-tract gene conversion, in comparison to controls expressing wild-type Rad51C. These long-tract events were not associated with crossing over between sister chromatids. Analysis of gene conversion tract lengths in CL-V4B cells lacking Rad51C revealed a bimodal frequency distribution, with almost all gene conversions being either less than 1 kb or greater than 3.2 kb in length. These results indicate that Rad51C plays a pivotal role in determining the "choice" between short- and long-tract gene conversion and in suppressing gene amplifications associated with sister chromatid recombination.

* Corresponding author. Mailing address: Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215. Phone: (617) 667-4252. Fax: (617) 667-0980. E-mail: rscully{at}bidmc.harvard.edu.

{triangledown} Published ahead of print on 5 September 2006.

Molecular and Cellular Biology, November 2006, p. 8075-8086, Vol. 26, No. 21
0270-7306/06/$08.00+0     doi:10.1128/MCB.01235-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Nagaraju, G., Hartlerode, A., Kwok, A., Chandramouly, G., Scully, R. (2009). XRCC2 and XRCC3 Regulate the Balance between Short- and Long-Tract Gene Conversions between Sister Chromatids. Mol. Cell. Biol. 29: 4283-4294 [Abstract] [Full Text]  
  • Fung, C. W., Mozlin, A. M., Symington, L. S. (2009). Suppression of the Double-Strand-Break-Repair Defect of the Saccharomyces cerevisiae rad57 Mutant. Genetics 181: 1195-1206 [Abstract] [Full Text]  
  • Pohl, T. J., Nickoloff, J. A. (2008). Rad51-Independent Interchromosomal Double-Strand Break Repair by Gene Conversion Requires Rad52 but Not Rad55, Rad57, or Dmc1. Mol. Cell. Biol. 28: 897-906 [Abstract] [Full Text]  
  • Mozlin, A. M., Fung, C. W., Symington, L. S. (2008). Role of the Saccharomyces cerevisiae Rad51 Paralogs in Sister Chromatid Recombination. Genetics 178: 113-126 [Abstract] [Full Text]  


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