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Checkpoint adaptation and recovery: back with Polo after the break.

机译：检查点适应和恢复：休息后返回Polo。

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摘要

S. cerevisiae cells that are unable to repair a double strand break ultimately escape the DNA damage checkpoint arrest and enter mitosis. This process called 'adaptation' depends on functional Cdc5, a Polo-like kinase, and was long thought to be limited to single-cell organisms. However, the recent finding that Xenopus extracts can adapt to a long-lasting stall in DNA replication indicates that checkpoint adaptation does also occur in multicellular organisms. Interestingly, the Xenopus Polo-like kinase (Plx1) plays an important role in this adaptation. To add to this, data from our laboratory have shown that the human Polo-like kinase (Plk1) is also required for cell cycle reentry following a DNA damage-induced arrest. But here, Plk1 was shown to be required for bona-fide checkpoint recovery, rather than adaptation. That is, Plk1 is required to restart the cell cycle once all of the damage is repaired and checkpoint signaling is turned off. While the target of Plx1 during adaptation is a component of the checkpoint machinery (Claspin), the target of Plk1 during recovery turns out to be a mitotic regulator (Wee1). Here, we discuss some of the remarkable similarities and subtle differences in the molecular mechanisms that control checkpoint adaptation and recovery, and the role of Polo-like kinases therein.
机译：不能修复双链断裂的酿酒酵母细胞最终逃脱了DNA损伤检查点的阻滞并进入有丝分裂。称为“适应”的过程取决于功能性Cdc5（一种Polo样激酶），长期以来被认为仅限于单细胞生物。但是，最近发现非洲爪蟾提取物可以适应DNA复制中的长期失速的发现表明，检查点适应也确实在多细胞生物中发生。有趣的是，非洲爪蟾Polo样激酶（Plx1）在这种适应中起着重要作用。此外，来自我们实验室的数据表明，DNA损伤诱导的阻滞后，细胞周期再进入也需要人类Polo样激酶（Plk1）。但是在这里，Plk1被证明是真正的检查点恢复而不是适应所必需的。也就是说，一旦修复了所有损坏并且关闭了检查点信令，就需要Plk1重新启动单元周期。尽管适应过程中Plx1的目标是检查点机制（Claspin）的组成部分，但恢复过程中Plk1的目标却是有丝分裂调节剂（Wee1）。在这里，我们讨论了控制检查点适应和恢复的分子机制中的一些显着相似性和微妙差异，以及其中的Polo样激酶的作用。

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