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首页> 外文期刊>Nucleic acids research >Mek1 stabilizes Hop1-Thr318 phosphorylation to promote interhomolog recombination and checkpoint responses during yeast meiosis
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Mek1 stabilizes Hop1-Thr318 phosphorylation to promote interhomolog recombination and checkpoint responses during yeast meiosis

机译：Mek1稳定Hop1-Thr318磷酸化，以促进酵母减数分裂过程中的同源重组和检查点响应

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摘要

Red1, Hop1 and Mek1 are three yeast meiosis-specific chromosomal proteins that uphold the interhomolog (IH) bias of meiotic recombination. Mek1 is also an effector protein kinase in a checkpoint that responds to aberrant DNA and/or axis structure. The activation of Mek1 requires Red1-dependent Hop1-Thr(T)318 phosphorylation, which is mediated by Mec1 and Tel1, the yeast homologs of the mammalian DNA damage sensor kinases ATR and ATM. As the ectopic expression of Mek1-glutathione S-transferase (GST) was shown to promote IH recombination in the absence of Mec1/Tel1-dependent checkpoint function, it was proposed that Mek1 might play dual roles during meiosis by directly phosphorylating targets that are involved in the recombination checkpoint. Here, we report that Mek1 has a positive feedback activity in the stabilization of Mec1/Tel1-mediated Hop1-T318 phosphorylation against the dephosphorylation mediated by protein phosphatase 4. Our results also reveal that GST-Mek1 or Mek1-GST further increases Hop1-T318 phosphorylation. This positive feedback function of Mek1 is independent of Mek1's kinase activity, but dependent on Mek1's forkhead-associated (FHA) domain and its arginine 51 residue. Arginine 51 directly mediates the interaction of Mek1-FHA and phosphorylated Hop1-T318. We suggest that the Hop1–Mek1 interaction is similar to the Rad53-Dun1 signaling pathway, which is mediated through the interaction of phosphorylated Rad53 and Dun1-FHA.
机译：Red1，Hop1和Mek1是三种酵母减数分裂特异的染色体蛋白，它们支持减数分裂重组的同源（IH）偏向。 Mek1在检查点中也是效应蛋白激酶，对异常的DNA和/或轴结构有反应。 Mek1的激活需要依赖Red1的Hop1-Thr（T）318磷酸化，这是由Mec1和Tel1（哺乳动物DNA损伤传感器激酶ATR和ATM的酵母同源物）介导的。由于在不存在依赖Mec1 / Tel1的检查点功能的情况下，Mek1-谷胱甘肽S-转移酶（GST）的异位表达可促进IH重组，因此提出Mek1在减数分裂过程中可能通过直接磷酸化相关靶标而发挥双重作用。在重组检查点。在这里，我们报告说，Mek1在稳定Mec1 / Tel1介导的Hop1-T318磷酸化对抗蛋白磷酸酶4介导的去磷酸化方面具有正反馈活性。我们的结果还表明，GST-Mek1或Mek1-GST进一步增加了Hop1-T318磷酸化。 Mek1的这种正反馈功能独立于Mek1的激酶活性，但取决于Mek1的叉头相关（FHA）域及其精氨酸51残基。精氨酸51直接介导Mek1-FHA和磷酸化的Hop1-T318的相互作用。我们建议，Hop1–Mek1的相互作用类似于Rad53-Dun1的信号通路，这是通过磷酸化的Rad53和Dun1-FHA的相互作用介导的。

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