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首页> 外文期刊>Genes & Genetic Systems >A novel role for Rad17 in homologous recombination
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A novel role for Rad17 in homologous recombination

机译：Rad17在同源重组中的新作用

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摘要

Replication checkpoint protein Rad17 senses DNA lesions during DNA replication and halts progression of replication fork. The cells derived from Bloom syndrome individuals show some defects in DNA replication. In order to investigate the functional relationship between the replication checkpoint protein Rad17 and BLM, which is the product of the causative gene of Bloom syndrome, we generated BLM/RAD17 double knockout (blm/rad17) cells using chicken DT40 cells. The blm/rad17 cells showed exaggerated growth defects as determined by analysis of their growth curves and plating efficiency compared to those of either of the single gene mutants. These defects seem to be due to an increase in DNA lesions that cause spontaneous cell death, suggesting that Rad17 and BLM execute different functions in the progression of replication forks. We also demonstrate that targeting integration was dramatically compromised by a lack of Rad17. In addition, the elevated frequency of sister chromatid exchange (SCE) due to homologous recombination in BLM knockout (blm) cells was greatly reduced by disruption of the RAD17 gene. Thus, in addition to its role in the replication checkpoint, Rad17 appears to play a role in homologous recombination.
机译：复制检查点蛋白Rad17在DNA复制过程中感知DNA损伤，并停止复制叉的进程。布鲁姆综合症个体的细胞在DNA复制中显示出一些缺陷。为了研究复制检查点蛋白Rad17和Bloom致病基因的产物BLM之间的功能关系，我们使用鸡DT40细胞生成了BLM / RAD17双敲除（blm / rad17）细胞。 blm / rad17细胞显示出过大的生长缺陷，这是通过分析其生长曲线和接种效率来确定的，与任何一个单基因突变体相比。这些缺陷似乎是由于引起自然细胞死亡的DNA损伤增加所致，这表明Rad17和BLM在复制叉的进程中执行不同的功能。我们还证明，缺乏Rad17大大损害了目标整合。另外，通过破坏RAD17基因，大大减少了由于BLM基因敲除（blm）细胞中的同源重组而导致的姊妹染色单体交换（SCE）的升高频率。因此，除了其在复制检查点中的作用外，Rad17似乎在同源重组中也起作用。

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