Targeted disruption of the Rad51 gene leads to lethality in embryonic mice
Targeted disruption of the Rad51 gene leads to lethality in embryonic mice
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DOI：
10.1073/pnas.93.13.6236
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发表时间：
1996-06-25
影响因子：
11.1
通讯作者：
Morita, T
中科院分区：
文献类型：
--
作者：
Tsuzuki, T;Fujii, Y;Morita, T
小鼠Rad51基因是哺乳动物中与大肠杆菌recA和酵母Rad51基因同源的基因，它们都参与同源重组和DNA修复。为了阐明Rad51蛋白的生理作用，我们将该基因定位于胚胎干（ES）细胞，对Rad51零突变的杂合小鼠进行杂交，并对其后代进行基因分型。148只幼崽中未发现纯合子（Rad51(-1)）幼崽，但在胚胎发育早期发现了少量Rad51（-1）胚胎。在选择性生长条件下未检测到双敲除的ES细胞。这些结果表明RAD51蛋白在细胞的增殖中起着至关重要的作用，纯合的RAD51零突变可以归类为细胞自主缺陷。植入前的致命突变会破坏基本的分子功能，从而干扰细胞活力。
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 inter-crossed and their offspring were genotyped. There were no homozygous (Rad51(-1-)) pups among 148 neonates examined but a few Rad51(-1-) 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.