Targeted disruption of the Rad51 gene leads to lethality in embryonic mice.

AUTOR(ES)

Tsuzuki, T

RESUMO

The mouse Rad51 gene is a mammalian homologue of the Escherichia coli recA and yeast RAD51 genes, both of which are involved in homologous recombination and DNA repair. To elucidate the physiological role of RAD51 protein, the gene was targeted in embryonic stem (ES) cells. Mice heterozygous for the Rad51 null mutation were intercrossed and their offspring were genotyped. There were no homozygous (Rad51-/-) pups among 148 neonates examined but a few Rad51-/- embryos were identified when examined during the early stages of embryonic development. Doubly knocked-out ES cells were not detected under conditions of selective growth. These results are interpreted to mean that RAD51 protein plays an essential role in the proliferation of cell. The homozygous Rad51 null mutation can be categorized in cell-autonomous defects. Pre-implantational lethal mutations that disrupt basic molecular functions will thus interfere with cell viability.

Documentos Relacionados

• Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality
• Genetic re-engineering of Saccharomyces cerevisiae RAD51 leads to a significant increase in the frequency of gene repair in vivo
• ATR disruption leads to chromosomal fragmentation and early embryonic lethality
• Targeted disruption of the Walker–Warburg syndrome gene Pomt1 in mouse results in embryonic lethality
• Disruption of muREC2/RAD51L1 in Mice Results in Early Embryonic Lethality Which Can Be Partially Rescued in a p53−/− Background