A Mutation in Mouse rad51 Results in an Early Embryonic Lethal That Is Suppressed by a Mutation in p53 | Zendy

DaeSik Lim | Zendy; Paul Hasty | Zendy

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A Mutation in Mouse rad51 Results in an Early Embryonic Lethal That Is Suppressed by a Mutation in p53

Author(s) -

DaeSik Lim,

Paul Hasty

Publication year - 1996

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.16.12.7133

Subject(s) - biology , mutant , rad51 , embryonic stem cell , mutation , microbiology and biotechnology , homologous recombination , saccharomyces cerevisiae , embryo , genetics , escherichia coli , programmed cell death , embryogenesis , gene , apoptosis

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.

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