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首页> 外文期刊>Cell cycle >The fate of metaphase kinetochores is weighed in the balance of SUMOylation during S phase.
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The fate of metaphase kinetochores is weighed in the balance of SUMOylation during S phase.

机译：在S期的SUMOylation平衡中，权衡中期动植物的命运。

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Genetic evidence suggests that conjugation of Small Ubiquitin-like Modifier proteins (SUMOs) plays an important role in kinetochore function, although the mechanism underlying these observations are poorly defined. We found that depletion of the SUMO protease SENP6 from HeLa cells causes chromosome misalignment, prolonged mitotic arrest and chromosome missegregation. Many inner kinetochore proteins (IKPs) were mis-localized in SENP6-depleted cells. This gross mislocalization of IKPs is due to proteolytic degradation of CENP-I and CENP-H via the SUMO targeted Ubiquitin Ligase (STUbL) pathway. Our findings show that SENP6 is a key regulator of inner kinetochore assembly that antagonizes the cellular STUbL pathway to protect IKPs from degradation during S phase. Here, we will briefly review the implications of our findings and present new data on how SUMOylation during S phase can control chromosome alignment in the subsequent metaphase.
机译：遗传学证据表明，小泛素样修饰蛋白（SUMO）的结合在动线粒体功能中起着重要作用，尽管这些观察结果的基础机制尚不明确。我们发现从HeLa细胞中消耗SUMO蛋白酶SENP6会导致染色体错位，延长的有丝分裂阻滞和染色体错聚。许多内部的线粒体蛋白（IKPs）在SENP6缺失的细胞中定位错误。 IKP的这种总的错误定位是由于经由SUMO靶向泛素连接酶（STUbL）途径的CENP-1和CENP-H的蛋白水解降解。我们的研究结果表明SENP6是内部动粒组装的关键调节剂，它拮抗细胞STUbL途径以保护IKP在S期不被降解。在这里，我们将简要回顾研究结果的含义，并提供有关S期SUMOylation如何控制后续中期染色体排列的新数据。

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