Format

Send to:

Choose Destination
See comment in PubMed Commons below
Mol Cell Biol. 1996 Dec;16(12):7133-43.

A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53.

Author information

  • 1Department 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.

PMID:
8943369
[PubMed - indexed for MEDLINE]
PMCID:
PMC231717
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk