Double-strand-break-induced homologous recombination in mammalian cells Journal Article

Authors: Johnson, R. D.; Jasin, M.
Article Title: Double-strand-break-induced homologous recombination in mammalian cells
Abstract: In mammalian cells, the repair of DNA double-strand breaks (DSBs) occurs by both homologous and non-homologous mechanisms. Indirect evidence, including that from gene targeting and random integration experiments, had suggested that non-homologous mechanisms were significantly more frequent than homologous ones. However, more recent experiments indicate that homologous recombination is also a prominent DSB repair pathway. These experiments show that mammalian cells use homologous sequences located at multiple positions throughout the genome to repair a DSB. However, template preference appears to be biased, with the sister chromatid being preferred by 2-3 orders of magnitude over a homologous or heterologous chromosome. The outcome of homologous recombination in mammalian cells is predominantly gene conversion that is not associated with crossing-over. The preference for the sister chromatid and the bias against crossing-over seen in mitotic mammalian cells may have developed in order to reduce the potential for genome alterations that could occur when other homologous repair templates are utilized. In attempts to understand further the mechanism of homologous recombination, the proteins that promote this process are beginning to be identified. To date, four mammalian proteins have been demonstrated conclusively to be involved in DSB repair by homologous recombination: Rad54, XRCC2, XRCC3 and BRCA1. This paper summarizes results from a number of recent studies.
Keywords: unclassified drug; nonhuman; conference paper; animal cell; dna recombination; mammalia; animals; dna damage; gene targeting; dna repair; sister chromatid; brca1 protein; animalia; dna strand breakage; gene conversion; recombination, genetic; rad54 protein; sister chromatid exchange; base sequence; genome; sequence homology; endonuclease; mammals; protein derivative; mammal cell; crossing over; non-homologous end-joining; dna template; deoxyribonucleases, type ii site-specific; protein xrcc2; protein xrcc3; priority journal; brcai; sister chromatid tumorigenesis
Journal Title: Biochemical Society Transactions
Volume: 29
Issue: 2
ISSN: 0300-5127
Publisher: Portland Press Ltd  
Date Published: 2001-05-01
Start Page: 196
End Page: 201
Language: English
DOI: 10.1042/0300-5127:0290196
PUBMED: 11356153
PROVIDER: scopus
Notes: Preseneted at the Colloquium on New Frontiers in DNA Repair; 2000 Dec 19-21; Brighton, England -- Source: Scopus
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MSK Authors
  1. Maria Jasin
    211 Jasin