Affiliation:
1. Department of Biochemistry and Molecular Biology, M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Abstract
RecA in Escherichia coli and its homolog, ScRad51 in Saccharomyces cerevisiae, are known to be essential for recombinational repair. The homolog of RecA and ScRad51 in mice, MmRad51, was mutated to determine its function. Mutant embryos arrested early during development. A decrease in cell proliferation, followed by programmed cell death and chromosome loss, was observed. Radiation sensitivity was demonstrated in trophectoderm-derived cells. Interestingly, embryonic development progressed further in a p53 null background; however, fibroblasts derived from double-mutant embryos failed to proliferate in tissue culture.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
515 articles.
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