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SIT4蛋白磷酸酶在G1晚期发挥作用,以促进细胞进入S期。

The SIT4 protein phosphatase functions in late G1 for progression into S phase.

作者信息

Sutton A, Immanuel D, Arndt K T

机构信息

Cold Spring Harbor Laboratory, New York 11724.

出版信息

Mol Cell Biol. 1991 Apr;11(4):2133-48. doi: 10.1128/mcb.11.4.2133-2148.1991.

Abstract

Saccharomyces cerevisiae strains containing temperature-sensitive mutations in the SIT4 protein phosphatase arrest in late G1 at the nonpermissive temperature. Order-of-function analysis shows that SIT4 is required in late G1 for progression into S phase. While the levels of SIT4 do not change in the cell cycle, SIT4 associates with two high-molecular-weight phosphoproteins in a cell-cycle-dependent fashion. In addition, we have identified a polymorphic gene, SSD1, that in some versions can suppress the lethality due to a deletion of SIT4 and can also partially suppress the phenotypic defects due to a null mutation in BCY1. The SSD1 protein is implicated in G1 control and has a region of similarity to the dis3 protein of Schizosaccharomyces pombe. We have also identified a gene, PPH2alpha, that in high copy number can partially suppress the growth defect of sit4 strains. The PPH2 alpha gene encodes a predicted protein that is 80% identical to the catalytic domain of mammalian type 2A protein phosphatases but also has an acidic amino-terminal extension not present in other phosphatases.

摘要

在SIT4蛋白磷酸酶中含有温度敏感突变的酿酒酵母菌株,在非允许温度下会在G1晚期停滞。功能顺序分析表明,SIT4在G1晚期是进入S期所必需的。虽然SIT4的水平在细胞周期中没有变化,但SIT4以细胞周期依赖性方式与两种高分子量磷蛋白结合。此外,我们鉴定出一个多态性基因SSD1,在某些版本中,它可以抑制由于SIT4缺失导致的致死性,也可以部分抑制由于BCY1基因无效突变导致的表型缺陷。SSD1蛋白与G1期调控有关,并且有一个区域与粟酒裂殖酵母的dis3蛋白相似。我们还鉴定出一个基因PPH2alpha,其高拷贝数可以部分抑制sit4菌株的生长缺陷。PPH2alpha基因编码一种预测的蛋白质,它与哺乳动物2A型蛋白磷酸酶的催化结构域有80%的同源性,但也有一个酸性的氨基末端延伸,这是其他磷酸酶所没有的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfda/359901/32683341e39c/molcellb00138-0374-a.jpg

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