An essential role of DmRad51/SpnA in DNA repair and meiotic checkpoint control
An essential role of DmRad51/SpnA in DNA repair and meiotic checkpoint control
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DOI：
10.1093/emboj/cdg564
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发表时间：
2003-11
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影响因子：
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通讯作者：
Eric Staeva-Vieira;Siuk Yoo;R. Lehmann
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文献类型：
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作者：
Eric Staeva-Vieira;Siuk Yoo;R. Lehmann
Rad 51是体细胞和生殖细胞减数分裂过程中双链DNA断裂（DSB）重组修复所必需的保守蛋白。酵母Rad 51突变体是可行的，但显示出减数分裂缺陷。在小鼠中，RAD 51缺失导致早期胚胎死亡，这表明在高等真核生物中，Rad 51是生存所必需的。在这里，我们报告了SpnA作为果蝇Rad 51基因的鉴定，其序列在5个已知的果蝇Rad 51样基因中与人类和酵母的Rad 51同源物最密切相关。DmRad 51/sture A无效突变体是可行的，但卵子发生被减数分裂重组检查点的激活所破坏。我们表明，减数分裂表型的结果，从无法有效地修复DSB。我们的研究进一步表明，在果蝇中，Rad 51依赖性同源重组途径对于索马中的DNA修复不是必需的，除非暴露于DNA损伤剂。因此，我们提出，在正常条件下，第二个，Rad 51独立的修复途径可以防止DNA损伤的致命影响。
Rad51 is a conserved protein essential for recombinational repair of double‐stranded DNA breaks (DSBs) in somatic cells and during meiosis in germ cells. Yeast Rad51 mutants are viable but show meiosis defects. In the mouse, RAD51 deletions cause early embryonic death, suggesting that in higher eukaryotes Rad51 is required for viability. Here we report the identification of SpnA as the Drosophila Rad51 gene, whose sequence among the five known Drosophila Rad51‐like genes is most closely related to the Rad51 homologs of human and yeast. DmRad51/spnA null mutants are viable but oogenesis is disrupted by the activation of a meiotic recombination checkpoint. We show that the meiotic phenotypes result from an inability to effectively repair DSBs. Our study further demonstrates that in Drosophila the Rad51‐dependent homologous recombination pathway is not essential for DNA repair in the soma, unless exposed to DNA damaging agents. We therefore propose that under normal conditions a second, Rad51‐independent, repair pathway prevents the lethal effects of DNA damage.