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PMID: 8943369 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

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

Molecular and cellular biology ·Vol. 16 ·No. 12 ·1996-12-00 ·Pages 7133-43

Lim DS, Hasty P

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.

MeSH Terms
Animals DNA-Binding Proteins/genetics Embryonic and Fetal Development/genetics Female Fetal Death/genetics Gene Expression Regulation, Developmental Mice Mutation Rad51 Recombinase Tumor Suppressor Protein p53/genetics
Chemicals
DNA-Binding Proteins Tumor Suppressor Protein p53 Rad51 Recombinase Rad51 protein, mouse
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Lim D S
Department of Biochemistry and Molecular Biology, M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Hasty P
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Article Info
Journal
Molecular and cellular biology
Abbr.
Mol Cell Biol
ISSN
0270-7306
Published
1996-12-00
Pages
7133-43
Language
English
Region
United States
NLM ID
8109087
PMCID
PMC231717
Subset
IM
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