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首页> 外文期刊>Molecular and Cellular Biology >Competition between the Rad50 Complex and the Ku Heterodimer Reveals a Role for Exo1 in Processing Double-Strand Breaks but Not Telomeres
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Competition between the Rad50 Complex and the Ku Heterodimer Reveals a Role for Exo1 in Processing Double-Strand Breaks but Not Telomeres

机译：Rad50复合体和Ku异源二聚体之间的竞争揭示了Exo1在处理双链断裂而不是端粒中的作用。

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The Mre11-Rad50-Nbs1(Xrs2) complex and the Ku70-Ku80 heterodimer are thought to compete with each other for binding to DNA ends. To investigate the mechanism underlying this competition, we analyzed both DNA damage sensitivity and telomere overhangs in Schizosaccharomyces pombe rad50-d, rad50-d pku70-d, rad50-d exo1-d, and pku70-d rad50-d exo1-d cells. We found that rad50 exo1 double mutants are more methyl methanesulfonate (MMS) sensitive than the respective single mutants. The MMS sensitivity of rad50-d cells was suppressed by concomitant deletion of pku70+. However, the MMS sensitivity of the rad50 exo1 double mutant was not suppressed by the deletion of pku70+. The G-rich overhang at telomere ends in taz1-d cells disappeared upon deletion of rad50+, but the overhang reappeared following concomitant deletion of pku70+. Our data suggest that the Rad50 complex can process DSB ends and telomere ends in the presence of the Ku heterodimer. However, the Ku heterodimer inhibits processing of DSB ends and telomere ends by alternative nucleases in the absence of the Rad50-Rad32 protein complex. While we have identified Exo1 as the alternative nuclease targeting DNA break sites, the identity of the nuclease acting on the telomere ends remains elusive.
机译：Mre11-Rad50-Nbs1（Xrs2）复合物和Ku70-Ku80异二聚体被认为彼此竞争结合DNA末端。为了研究这种竞争的机制，我们分析了裂殖酵母rad50-d ， rad50-d pku70-d ， rad50- d exo1-d 和 pku70-d rad50-d exo1-d 细胞。我们发现 rad50 exo1 双重突变体比相应的单个突变体对甲烷磺酸甲酯（MMS）的敏感性更高。 rad50-d 细胞的MMS敏感性可通过同时缺失 pku70 + 来抑制。但是， rad50 exo1 双重突变体的MMS敏感性并未被 pku70 + 的缺失所抑制。 rad50 + 缺失后， taz1-d 细胞端粒末端的富含G的突出物消失，但同时缺失< em> pku70 + 。我们的数据表明，在Ku异二聚体存在下，Rad50复合物可以处理DSB末端和端粒末端。但是，在不存在Rad50-Rad32蛋白复合物的情况下，Ku异二聚体通过其他核酸酶抑制DSB末端和端粒末端的加工。虽然我们已经确定Exo1是靶向DNA断裂位点的替代核酸酶，但作用于端粒末端的核酸酶的身份仍然难以捉摸。

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