MEK1 通过失活 Myt1 来调节哺乳动物细胞的高尔基体膜断裂和有丝分裂进入。
MEK1 inactivates Myt1 to regulate Golgi membrane fragmentation and mitotic entry in mammalian cells.
机构信息
Cell and Developmental Biology Programme, Centre for Genomic Regulation, Barcelona, Spain.
出版信息
EMBO J. 2013 Jan 9;32(1):72-85. doi: 10.1038/emboj.2012.329. Epub 2012 Dec 14.
The pericentriolar stacks of Golgi cisternae are separated from each other in G2 and fragmented extensively during mitosis. MEK1 is required for Golgi fragmentation in G2 and for the entry of cells into mitosis. We now report that Myt1 mediates MEK1's effects on the Golgi complex. Knockdown of Myt1 by siRNA increased the efficiency of Golgi complex fragmentation by mitotic cytosol in permeabilized and intact HeLa cells. Myt1 knockdown eliminated the requirement of MEK1 in Golgi fragmentation and alleviated the delay in mitotic entry due to MEK1 inhibition. The phosphorylation of Myt1 by MEK1 requires another kinase but is independent of RSK, Plk, and CDK1. Altogether our findings reveal that Myt1 is inactivated by MEK1 mediated phosphorylation to fragment the Golgi complex in G2 and for the entry of cells into mitosis. It is known that Myt1 inactivation is required for CDK1 activation. Myt1 therefore is an important link by which MEK1 dependent fragmentation of the Golgi complex in G2 is connected to the CDK1 mediated breakdown of Golgi into tubules and vesicles in mitosis.
中心粒堆叠高尔基体潴泡在 G2 期彼此分离，并在有丝分裂期间广泛碎片化。MEK1 对于 G2 期高尔基体碎片化以及细胞进入有丝分裂是必需的。我们现在报告说，Myt1 介导 MEK1 对高尔基体复合物的作用。用 siRNA 敲低 Myt1 增加了有丝分裂细胞质在通透和完整的 HeLa 细胞中使高尔基体复合物碎片化的效率。Myt1 敲低消除了 MEK1 在高尔基体碎片化中的作用，并减轻了由于 MEK1 抑制而导致的有丝分裂进入的延迟。Myt1 由 MEK1 磷酸化需要另一种激酶，但不依赖于 RSK、Plk 和 CDK1。总之，我们的发现表明，Myt1 通过 MEK1 介导的磷酸化失活，在 G2 期碎片化高尔基体复合物，并促进细胞进入有丝分裂。已知 Myt1 失活是 CDK1 激活所必需的。因此，Myt1 是将 MEK1 依赖性高尔基体在 G2 期的碎片化与 CDK1 介导的高尔基体在有丝分裂中解聚为小管和囊泡连接起来的重要环节。
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