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Molecular and Cellular Biology, April 2001, p. 2858-2866, Vol. 21, No. 8
CREST Research Project, Radiation Genetics,
Faculty of Medicine,1 and Radiation
Biology Center,3 Kyoto University, Sakyo-ku,
Kyoto 606-8501, and CREST, JST (Japan Science and Technology),
Kawaguchi,2 Japan; Life Sciences
Division, Lawrence Berkeley National Laboratory, Berkeley, California
947204; and Biology and Biotechnology
Research Program, Lawrence Livermore National Laboratory, Livermore,
California 95441-08085
Received 19 September 2000/Returned for modification 24 October
2000/Accepted 29 December 2000
The Rad51 protein, a eukaryotic homologue of Escherichia
coli RecA, plays a central role in both mitotic and meiotic
homologous DNA recombination (HR) in Saccharomyces
cerevisiae and is essential for the proliferation of vertebrate
cells. Five vertebrate genes, RAD51B, -C,
and -D and XRCC2 and -3,
are implicated in HR on the basis of their sequence similarity to Rad51
(Rad51 paralogs). We generated mutants deficient in each of these
proteins in the chicken B-lymphocyte DT40 cell line and report here the
comparison of four new mutants and their complemented derivatives with
our previously reported rad51b mutant. The Rad51 paralog
mutations all impair HR, as measured by targeted integration and sister chromatid exchange. Remarkably, the mutant cell lines all exhibit very
similar phenotypes: spontaneous chromosomal aberrations, high
sensitivity to killing by cross-linking agents (mitomycin C and
cisplatin), mild sensitivity to gamma rays, and significantly attenuated Rad51 focus formation during recombinational repair after
exposure to gamma rays. Moreover, all mutants show partial correction
of resistance to DNA damage by overexpression of human Rad51. We
conclude that the Rad51 paralogs participate in repair as a functional
unit that facilitates the action of Rad51 in HR.
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.8.2858-2866.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Chromosome Instability and Defective
Recombinational Repair in Knockout Mutants of the Five Rad51
Paralogs

*
Corresponding author. Mailing address: CREST Research
Project, Radiation Genetics, Faculty of Medicine, Kyoto University, Konoe Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Phone: 81-75-753-4410. Fax: 81-75-753-4419. E-mail:
stakeda{at}rg1.rg.med.kyoto-u.ac.jp.
Present address: Department of Immunology and Molecular Genetics,
Kawasaki Medical School, Kurashiki 701-0192, Japan.
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