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首页> 外文期刊>Cellular Signalling >The GTP-binding protein G(i alpha) translocates to kinetochores and regulates the M-G(1) cell cycle transition of Swiss 3T3 cells
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The GTP-binding protein G(i alpha) translocates to kinetochores and regulates the M-G(1) cell cycle transition of Swiss 3T3 cells

机译：GTP结合蛋白G（i alpha）易位到动植物，并调节Swiss 3T3细胞的M-G（1）细胞周期转变

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The receptor-generated signals that are responsible for driving the cell cycle are incompletely characterised in mammalian cells. It is clear, however, that the cellular messenger systems that stimulate DNA synthesis and mitosis are separable. These are interwoven with biochemical checkpoints that ensure that processes, such as chromosomal replication and microtubule attachment to duplicated chromosomes, are complete before the following phase of the cell cycle is initiated. In some cells, activation of DNA synthesis by factors such as LPA and serum has been shown to require the GTP-binding protein G(i). We have found that G(i) plays an additional role in mitosis activated by both 7-transmembrane receptors and tyrosine kinase receptors, and that this involves the translocation of the alpha-subunit of G(i) (G(i alpha)) to the nucleus. Here we show by confocal microscopy that G(i alpha) migrates to the nucleus near the onset of mitosis in serum-activated Swiss 3T3 cells and binds to the kinetochore region of replicated chromosomes. Inhibition of G(i) function with pertussis toxin had no effect on the induction of DNA synthesis by serum, but cell proliferation was inhibited. Flow cytometric analysis showed that this resulted from retardation of the transition through mitosis and into G(1). Additionally, pertussis toxin impaired the activity of p34(cdc2), a cyclin-dependent kinase involved in the transition from M-phase to G(1), but not the S-phase cyclin, cyclin E. These data show that the G-protein G(i) has a key role in the regulation of mitosis in fibroblasts. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 27]
机译：在哺乳动物细胞中，不完全表征负责驱动细胞周期的受体产生的信号。但是，很明显，刺激DNA合成和有丝分裂的细胞信使系统是可分离的。这些与生化检查点交织在一起，以确保在启动细胞周期的下一阶段之前，完成诸如染色体复制和微管附着到重复染色体的过程。在某些细胞中，已经证明通过LPA和血清等因子激活DNA合成需要GTP结合蛋白G（i）。我们发现，G（i）在由7个跨膜受体和酪氨酸激酶受体激活的有丝分裂中起着额外的作用，并且这涉及G（i）的α-亚基（G（i alpha））向核。在这里，我们通过共聚焦显微镜显示，G（i alpha）迁移至血清激活的Swiss 3T3细胞中有丝分裂发作附近的核，并与复制染色体的动粒区结合。百日咳毒素抑制G（i）功能对血清诱导DNA合成没有影响，但细胞增殖受到抑制。流式细胞仪分析表明，这是由于有丝分裂过渡到G（1）的延迟所致。此外，百日咳毒素会破坏p34（cdc2）的活性，p34（cdc2）是一种细胞周期蛋白依赖性激酶，参与从M期向G（1）的转变，但不影响S期细胞周期蛋白cyclinE。这些数据表明，G-蛋白G（i）在成纤维细胞的有丝分裂调控中起关键作用。 （C）2000 Elsevier Science Inc.保留所有权利。 [参考：27]

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