Suppression of mutagenesis by Rad51D-mediated homologous recombination [electronic resource].
- Washington, D.C. : United States. Dept. of Energy, 2005. and Oak Ridge, Tenn. : Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy.
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- PDF-file: 37 pages; size: 0 Kbytes
- Additional Creators:
- Lawrence Berkeley National Laboratory, United States. Department of Energy, and United States. Department of Energy. Office of Scientific and Technical Information
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- Free-to-read Unrestricted online access
- Homologous recombinational repair (HRR) restores chromatid breaks arising during DNA replication and prevents chromosomal rearrangements that can occur from the misrepair of such breaks. In vertebrates, five Rad51 paralogs are identified that contribute in a nonessential but critical manner to HRR efficiency. We constructed and characterized a Rad51D knockout cell line in widely studied CHO cells. The rad51d mutant (51D1) displays sensitivity to a wide spectrum of induced DNA damage, indicating the broad relevance of HRR to genotoxicity. Untreated 51D1 cells exhibit ≈5-fold elevated chromosomal breaks, a 12-fold increased rate of hprt mutation, and 4- to 10-fold increased rates of gene amplification at the dhfr and CAD loci, respectively. These results explicitly show the quantitative importance of HHR in preventing these types genetic alterations, which are associated with carcinogenesis. Thus, HRR copes in an error-free manner with spontaneous DNA damage encountered during DNA replication, and Rad51D is essential for this fidelity.
- Published through SciTech Connect., 11/15/2005., "ucrl-jrnl-217120", Nucleic Acids Research 34 5 ISSN 0305-1048; NARHAD FT, and Thompson, L H; Wilson, P F; Salazar, E P; Tebbs, R S; Nagasawa, H; Hinz, J M; Nham, P B; Urbin, S S.
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