Disruption of muREC2/RAD51L1 in Mice Results in Early Embryonic Lethality Which Can Be Partially Rescued in a p53−/− Background

AUTOR(ES)

Shu, Zhigang

FONTE

American Society for Microbiology

RESUMO

muREC2/RAD51L1 is a radiation-inducible gene that regulates cell cycle progression. To elucidate the biological function of muREC2/RAD51L1, the gene was disrupted in embryonic stem cells by homologous recombination. Mice heterozygous for muREC2/RAD51L1 appear normal and fertile; however, no homozygous pups were born after interbreeding of heterozygous mice. Timed pregnancy studies showed that homozygous mutant embryos were severely retarded in growth as early as ca. 5 days gestation (E5.5) and were completely resorbed by E8.5. Mutant blastocyst outgrowth was also severely impaired in a double-knockout embryo, but embryonic development did progress further in a p53-null background. These results suggest that muREC2/RAD51L1 plays a role in cell proliferation and early embryonic development, perhaps through interaction with p53.

Documentos Relacionados

• Targeted disruption of the Rad51 gene leads to lethality in embryonic mice.
• A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53.
• p53 Accumulation, defective cell proliferation, and early embryonic lethality in mice lacking tsg101
• p53 is linked directly to homologous recombination processes via RAD51/RecA protein interaction.
• Complete antithrombin deficiency in mice results in embryonic lethality