Disruption of muREC2/RAD51L1 in mice results in early embryonic lethality which can Be partially rescued in a p53(-/-) background

Mol Cell Biol. 1999 Dec;19(12):8686-93. doi: 10.1128/MCB.19.12.8686.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blastomeres / cytology
  • Cells, Cultured
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Embryonic and Fetal Development
  • Female
  • Gene Deletion
  • Gene Targeting
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Phenotype
  • Pregnancy
  • Proteins / genetics
  • Proteins / physiology*
  • Rad51 Recombinase
  • Recombination, Genetic
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • DNA-Binding Proteins
  • Proteins
  • RAD51B protein, human
  • Tumor Suppressor Protein p53
  • Rad51 Recombinase
  • Rad51 protein, mouse