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Homologous recombination is essential for RAD51 up-regulation in Saccharomyces cerevisiae following DNA crosslinking damage

机译:DNA交联破坏后同源重组对于酿酒酵母中RAD51上调至关重要

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摘要

We have determined the kinetics of up-regulation of the homologous recombination gene RAD51, one of the genes induced following DNA damage in isogenic haploid DNA repair-deficient mutants of Saccharomyces cerevisiae, using treatment with the DNA crosslinking agent 8-methoxypsoralen. We show that RAD51 is up-regulated concomitantly, although independently, with a shift from the G1 cell cycle phase to G2/M arrest. This up-regulation is absent in homologous recombination repair-deficient mutants and increased in mutants deficient in nucleotide excision repair and polζ-dependent translesion synthesis. We demonstrate that the Rad53-dependent DNA damage signal transduction cascade is active in RAD51 non-inducing mutants. However, when independently eliminated, it too abolishes RAD51 up-regulation. We present a model in which RAD51 up-regulation requires two signals: one depending on the Rad53-dependent DNA damage signal transduction cascade and the other on homologous recombination repair.
机译:我们已经确定了同源重组基因RAD51的上调动力学,该基因是在酿酒酵母的同基因单倍体DNA修复缺陷型突变体中使用DNA交联剂8-甲氧基补骨脂素处理后被DNA损伤后诱导的基因之一。我们显示,RAD51是伴随上调的,尽管独立地是从G1细胞周期期向G2 / M停滞期的转移。同源重组修复缺陷型突变体中不存在这种上调,而核苷酸切除修复和polζ依赖性转基因合成缺陷型突变体中却没有这种上调。我们证明了Rad53依赖的DNA损伤信号转导级联在RAD51非诱导突变体中很活跃。但是,当独立消除它时,它也会消除RAD51的上调。我们提出了一个模型,其中RAD51上调需要两个信号:一个取决于Rad53依赖的DNA损伤信号转导级联,另一个取决于同源重组修复。

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