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A role for RAD54B in homologous recombination in human cells
Author(s) -
Miyagawa Kiyoshi,
Tsuruga Takanori,
Kinomura Aiko,
Usui Kiyomi,
Katsura Mari,
Tashiro Satoshi,
Mishima Hiromu,
Tanaka Kozo
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/21.1.175
Subject(s) - library science , medicine , computer science
In human somatic cells, homologous recombination is a rare event. To facilitate the targeted modification of the genome for research and gene therapy applications, efforts should be directed toward understanding the molecular mechanisms of homologous recombination in human cells. Although human genes homologous to members of the RAD52 epistasis group in yeast have been identified, no genes have been demonstrated to play a role in homologous recombination in human cells. Here, we report that RAD54B plays a critical role in targeted integration in human cells. Inactivation of RAD54B in a colon cancer cell line resulted in severe reduction of targeted integration frequency. Sensitivity to DNA‐damaging agents and sister‐chromatid exchange were not affected in RAD54B ‐deficient cells. Parts of these phenotypes were similar to those of Saccharomyces cerevisiae tid1/rdh54 mutants, suggesting that RAD54B may be a human homolog of TID1/RDH54 . In yeast, TID1/RDH54 acts in the recombinational repair pathway via roles partially overlapping those of RAD54 . Our findings provide the first genetic evidence that the mitotic recombination pathway is functionally conserved from yeast to humans.