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G2期向有丝分裂期转变的调控。

Regulation of the G2-mitosis transition.

作者信息

Feilotter H, Lingner C, Rowley R, Young P G

机构信息

Cold Spring Harbor Laboratory, NY 11724.

出版信息

Biochem Cell Biol. 1992 Oct-Nov;70(10-11):954-71. doi: 10.1139/o92-140.

Abstract

The cell cycle is regulated by pathways composed of a dependent series of steps, by timers, and by checkpoint controls which ensure the completion of one event before the initiation of another. This review focuses on the regulation of the initiation of mitosis, with particular emphasis on the regulation of p34cdc2 activity at this point in the cell cycle. The review draws on data from various organisms, but strongly emphasizes the genetic framework as seen in the fission yeast Schizosaccharomyces pombe and the biology and biochemistry of maturation promoting factor in frog oocytes. An attempt is made to include all known genes and proteins where a link can be made to the initiation event. The nutritional size control and its major known controlling elements, the wee1/mik1 protein kinases, and cdc25 protein tyrosine phosphatase are considered in detail along with their regulation. In addition, the checkpoint control pathways which mediate G2 delay in response to failure of DNA replication or DNA damage are examined.

摘要

细胞周期由一系列相互依赖的步骤所组成的通路、定时器以及检查点控制来调节,这些检查点控制可确保一个事件完成后才开始另一个事件。本综述着重于有丝分裂起始的调控,特别强调细胞周期这一阶段中p34cdc2活性的调控。该综述借鉴了来自各种生物体的数据,但重点突出了裂殖酵母粟酒裂殖酵母中的遗传框架以及蛙卵母细胞中成熟促进因子的生物学和生物化学。我们试图纳入所有已知的、与起始事件有联系的基因和蛋白质。详细讨论了营养大小控制及其主要已知调控元件wee1/mik1蛋白激酶和cdc25蛋白酪氨酸磷酸酶及其调控。此外,还研究了介导G2期延迟以应对DNA复制失败或DNA损伤的检查点控制通路。

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