A MUTATION IN MOUSE RAD51 RESULTS IN AN EARLY EMBRYONIC LETHAL THAT IS SUPPRESSED BY A MUTATION IN P53

RecA in Escherichia coli and its homolog, ScRad51 in Saccharomyces cer evisiae, are known to be essential for recombinational repair. The hom olog of RecA and ScRad51 in mice, MmRad51, was mutated to determine it s function. Mutant embryos arrested early during development. A decrea se in cell proliferation, followed by programmed cell death and chromo some loss, was observed. Radiation sensitivity was demonstrated in tro phectoderm-derived cells. Interestingly, embryonic development progres sed further in a p53 null background; however, fibroblasts derived fro m double-mutant embryos failed to proliferate in tissue culture.