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酵母中Ras/cAMP途径对G1细胞周期蛋白活性的抑制作用。

Inhibition of G1 cyclin activity by the Ras/cAMP pathway in yeast.

作者信息

Tokiwa G, Tyers M, Volpe T, Futcher B

机构信息

Cold Spring Harbor Laboratory, New York 11724.

出版信息

Nature. 1994 Sep 22;371(6495):342-5. doi: 10.1038/371342a0.

Abstract

In the yeast Saccharomyces cerevisiae, commitment to cell division (Start) requires growth to a critical cell size. The G1 cyclins Cln1, Cln2 and Cln3 activate the Cdc28 protein kinase and are rate-limiting activators of Start. When glucose is added to cells growing in a poor carbon source, the critical cell size required for Start is reset from a small to a large size. In yeast, glucose acts through Ras proteins to stimulate adenylyl cyclase, activating the three cyclic AMP-dependent protein kinases Tpk1, Tpk2 and Tpk3 (refs 8, 9). We find that stimulation of the Ras/cAMP pathway represses expression of CLN1, CLN2 and co-regulated genes, inhibiting Start. This helps explain the increase in critical size when cells are shifted from poor to rich medium. This connection between the molecules controlling growth (Ras/cAMP) and those controlling division (cyclins) helps explain how division is co-ordinated with growth.

摘要

在酿酒酵母中,进入细胞分裂(起始点)需要生长到临界细胞大小。G1 细胞周期蛋白 Cln1、Cln2 和 Cln3 激活 Cdc28 蛋白激酶,是起始点的限速激活因子。当向在贫碳源中生长的细胞添加葡萄糖时,起始点所需的临界细胞大小从小尺寸重置为大尺寸。在酵母中,葡萄糖通过 Ras 蛋白作用于刺激腺苷酸环化酶,激活三种环磷酸腺苷依赖性蛋白激酶 Tpk1、Tpk2 和 Tpk3(参考文献 8、9)。我们发现,刺激 Ras/cAMP 途径会抑制 CLN1、CLN2 及共同调控基因的表达,从而抑制起始点。这有助于解释当细胞从贫培养基转移到富培养基时临界大小的增加。这种控制生长(Ras/cAMP)的分子与控制分裂(细胞周期蛋白)的分子之间的联系,有助于解释分裂如何与生长协调。

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