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

Teruhisa Tsuzuki, Yoshimitsu Fujii, Kunihiko Sakumi, Yohei Tominaga, Kazuki Nakao, Mutsuo Sekiguchi, Aizo Matsushiro, Yasuhide Yoshimura, Takashi Morita

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683 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)6236-6240
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number13
Publication statusPublished - Jun 25 1996

All Science Journal Classification (ASJC) codes

  • General


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