Nuclear pore formation but not nuclear growth is governed by cyclin-dependent kinases (Cdks) during interphase
Nuclear pore formation but not nuclear growth is governed by cyclin-dependent kinases (Cdks) during interphase
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DOI：
10.1038/nsmb.1878
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发表时间：
2010-09-01
影响因子：
16.8
通讯作者：
Imamoto, Naoko
中科院分区：
文献类型：
--
作者：
Maeshima, Kazuhiro;Iino, Haruki;Imamoto, Naoko
在细胞分裂的间期，细胞核体积和核孔复合物（NPCs）的数量几乎增加一倍。这些事件是如何与细胞周期协调的，人们知之甚少，特别是在哺乳动物细胞中。我们在此报道，基于新开发的鼻咽癌形成可视化技术，周期蛋白依赖性激酶（Cdks），特别是Cdk1和Cdk2，促进人类分裂细胞间期鼻咽癌的形成。Cdk似乎推动了NPC形成的早期步骤，因为Cdk抑制抑制了“新生孔隙”的产生，我们认为这是形成过程中未成熟的NPC。与此一致的是，Cdk抑制干扰了一些核孔蛋白的正常表达和定位，包括Elys/Mel-28，从而触发有丝分裂后NPC组装。值得注意的是，Cdk抑制并未显著影响核生长，这表明间期NPC的形成和核生长具有不同的调节机制。
Nuclear volume and the number of nuclear pore complexes (NPCs) on the nucleus almost double during interphase in dividing cells. How these events are coordinated with the cell cycle is poorly understood, particularly in mammalian cells. We report here, based on newly developed techniques for visualizing NPC formation, that cyclin-dependent kinases (Cdks), especially Cdk1 and Cdk2, promote interphase NPC formation in human dividing cells. Cdks seem to drive an early step of NPC formation because Cdk inhibition suppressed generation of 'nascent pores', which we argue are immature NPCs under the formation process. Consistent with this, Cdk inhibition disturbed proper expression and localization of some nucleoporins, including Elys/Mel-28, which triggers postmitotic NPC assembly. Strikingly, Cdk suppression did not notably affect nuclear growth, suggesting that interphase NPC formation and nuclear growth have distinct regulation mechanisms.