REG1 binds to protein phosphatase type 1 and regulates glucose repression in Saccharomyces cerevisiae.

REG1 binds to protein phosphatase type 1 and regulates glucose repression in Saccharomyces cerevisiae.
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REG1 与 1 型蛋白磷酸酶结合并调节酿酒酵母中的葡萄糖抑制。

DOI:
10.1002/j.1460-2075.1995.tb00282.x
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发表时间:
1995
期刊:
The EMBO journal
影响因子:
--
通讯作者:
Carlson,M
Carlson,M
中科院分区:
--
文献类型:
--
作者:
Tu,J;Carlson,M

文献摘要

被引文献

相似文献

蛋白磷酸酶1(PP1)由酿酒酵母的必需基因GLC7编码。GLC7磷酸酶是葡萄糖抑制所必需的,它的功能似乎与SNF1蛋白激酶有拮抗作用。此前,我们鉴定了一种突变,glc7-T152K,它可以缓解葡萄糖抑制,但不会干扰GLC7在糖原代谢中的功能。我们认为突变的GLC7T152K磷酸酶在与指导PP1参与葡萄糖抑制机制的调节亚基的相互作用中存在缺陷。在这里,我们提出的证据表明,REG1,一种葡萄糖抑制所需的蛋白质,就是这样一个调节亚基。我们发现REG1在物理上与GLC7有关。在双杂交系统中,REG1与GLC7强烈且特异地相互作用,REG1和GLC7融合蛋白从细胞提取液中免疫共沉淀。此外,REG1融合蛋白的过表达抑制了葡萄糖抑制中的glc7-T152K突变缺陷。这一点和其他遗传证据表明,这两种蛋白质在调节葡萄糖抑制方面共同发挥作用。这些结果表明,REG1是PP1的一个调节亚单位,其活性针对葡萄糖抑制调节途径中的蛋白质。
Protein phosphatase type 1 (PP1) is encoded by GLC7, an essential gene in Saccharomyces cerevisiae. The GLC7 phosphatase is required for glucose repression and appears to function antagonistically to the SNF1 protein kinase. Previously, we characterized a mutation, glc7‐T152K, that relieves glucose repression but does not interfere with the function of GLC7 in glycogen metabolism. We proposed that the mutant GLC7T152K phosphatase is defective in its interaction with a regulatory subunit that directs participation of PP1 in the glucose repression mechanism. Here, we present evidence that REG1, a protein required for glucose repression, is one such regulatory subunit. We show that REG1 is physically associated with GLC7. REG1 interacts with GLC7 strongly and specifically in the two‐hybrid system, and REG1 and GLC7 fusion proteins co‐immunoprecipitate from cell extracts. Moreover, overexpression of a REG1 fusion protein suppresses the glc7‐T152K mutant defect in glucose repression. This and other genetic evidence indicate that the two proteins function together in regulating glucose repression. These results suggest that REG1 is a regulatory subunit of PP1 that targets its activity to proteins in the glucose repression regulatory pathway.