Tu J, Carlson M
Institute of Cancer Research, Columbia University, New York, New York 10032.
Mol Cell Biol. 1994 Oct;14(10):6789-96. doi: 10.1128/mcb.14.10.6789-6796.1994.
We cloned the GLC7/DIS2S1 gene by complementation of the cid1-226 mutation, which relieves glucose repression in Saccharomyces cerevisiae. GLC7 encodes the catalytic subunit of type 1 protein phosphatase (PP1). Genetic analysis and sequencing showed that cid1-226 is an allele of GLC7, now designated glc7-T152K, which alters threonine 152 to lysine. We also show that the glc7-1 and glc7-T152K alleles cause distinct phenotypes: glc7-1 causes a severe defect in glycogen accumulation but does not relieve glucose repression, whereas glc7-T152K does not prevent glycogen accumulation. These findings are discussed in light of evidence that interaction with different regulatory or targeting subunits directs the participation of PP1 in diverse cellular regulatory mechanisms. Finally, genetic studies suggest that PP1 functions antagonistically to the SNF1 protein kinase in the regulatory response to glucose.
我们通过互补cid1 - 226突变克隆了GLC7/DIS2S1基因,该突变可缓解酿酒酵母中的葡萄糖阻遏。GLC7编码1型蛋白磷酸酶(PP1)的催化亚基。遗传分析和测序表明,cid1 - 226是GLC7的一个等位基因,现命名为glc7 - T152K,它将苏氨酸152变为赖氨酸。我们还表明,glc7 - 1和glc7 - T152K等位基因会导致不同的表型:glc7 - 1在糖原积累方面存在严重缺陷,但不能缓解葡萄糖阻遏,而glc7 - T152K不会阻止糖原积累。鉴于与不同调节或靶向亚基的相互作用指导PP1参与多种细胞调节机制的证据,对这些发现进行了讨论。最后,遗传研究表明,在对葡萄糖的调节反应中,PP1与SNF1蛋白激酶起拮抗作用。