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首页> 外文期刊>Nature >Cdc48/p97 promotes reformation of the nucleus by extracting the kinase Aurora B from chromatin
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Cdc48/p97 promotes reformation of the nucleus by extracting the kinase Aurora B from chromatin

机译：Cdc48 / p97通过从染色质中提取激酶Aurora B来促进细胞核的重建

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摘要

During division of metazoan cells, the nucleus disassembles to allow chromosome segregation, and then reforms in each daughter cell. Reformation of the nucleus involves chromatin decondensa-tion and assembly of the double-membrane nuclear envelope around the chromatin; however, regulation of the process is still poorly understood. In vitro, nucleus formation requires p97 (ref. 3), a hexameric ATPase implicated in membrane fusion and ubiquitin-dependent processes. However, the role and relevance of p97 in nucleus formation have remained controversial. Here we show that p97 stimulates nucleus reformation by inactivating the chromatin-associated kinase Aurora B. During mitosis, Aurora B inhibits nucleus reformation by preventing chromosome decon-densation and formation of the nuclear envelope membrane. During exit from mitosis, p97 binds to Aurora B after its ubiqui-tylation and extracts it from chromatin. This leads to inactivation of Aurora B on chromatin, thus allowing chromatin decondensa-tion and nuclear envelope formation. These data reveal an essential pathway that regulates reformation of the nucleus after mitosis and defines ubiquitin-dependent protein extraction as a common mechanism of Cdc48/p97 activity also during nucleus formation.
机译：在后生细胞分裂过程中，细胞核分解以允许染色体分离，然后在每个子细胞中重新形成。核的重整涉及染色质的缩聚和染色质周围的双膜核膜的组装。但是，对该过程的调节仍然知之甚少。在体外，细胞核的形成需要p97（参考文献3），这是一种涉及膜融合和泛素依赖性过程的六聚体ATPase。然而，p97在细胞核形成中的作用和相关性仍存在争议。在这里，我们显示p97通过使染色质相关激酶Aurora B失活来刺激细胞核再造。在有丝分裂期间，Aurora B通过防止染色体解聚和核被膜的形成来抑制细胞核再造。在有丝分裂退出过程中，p97泛素化后与Aurora B结合并从染色质中提取。这导致染色质上的Aurora B失活，从而使染色质脱凝并形成核包膜。这些数据揭示了调节有丝分裂后核重组的必经途径，并将泛素依赖性蛋白提取定义为在核形成过程中Cdc48 / p97活性的常见机制。

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