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Double-strand break repair in the absence of RAD51 in yeast: a possible role for break-induced DNA replication.酵母中缺乏RAD51时的双链断裂修复：断裂诱导的DNA复制的可能作用。
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小鼠rad51基因的一个突变会导致早期胚胎致死，而这种致死效应会被p53基因的一个突变所抑制。

A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53.

作者信息

Lim D S, Hasty P

机构信息

Department of Biochemistry and Molecular Biology, M.D. Anderson Cancer Center, Houston, Texas 77030, USA.

出版信息

Mol Cell Biol. 1996 Dec;16(12):7133-43. doi: 10.1128/MCB.16.12.7133.

DOI:10.1128/MCB.16.12.7133
PMID:8943369
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC231717/
Abstract

RecA in Escherichia coli and its homolog, ScRad51 in Saccharomyces cerevisiae, are known to be essential for recombinational repair. The homolog of RecA and ScRad51 in mice, MmRad51, was mutated to determine its function. Mutant embryos arrested early during development. A decrease in cell proliferation, followed by programmed cell death and chromosome loss, was observed. Radiation sensitivity was demonstrated in trophectoderm-derived cells. Interestingly, embryonic development progressed further in a p53 null background; however, fibroblasts derived from double-mutant embryos failed to proliferate in tissue culture.

摘要

已知大肠杆菌中的RecA及其在酿酒酵母中的同源物ScRad51对重组修复至关重要。对小鼠中RecA和ScRad51的同源物MmRad51进行突变以确定其功能。突变胚胎在发育早期停滞。观察到细胞增殖减少，随后是程序性细胞死亡和染色体丢失。在滋养外胚层来源的细胞中表现出辐射敏感性。有趣的是，在p53基因缺失的背景下胚胎发育进一步进行；然而，来自双突变胚胎的成纤维细胞在组织培养中无法增殖。