Toda T, Cameron S, Sass P, Wigler M
Cold Spring Harbor Laboratory, New York 11724.
Genes Dev. 1988 May;2(5):517-27. doi: 10.1101/gad.2.5.517.
A new gene, SCH9, was isolated from Saccharomyces cerevisiae by its ability to complement a cdc25ts mutation. Sequence analysis indicates that it encodes a 90,000-dalton protein with a carboxy-terminal domain homologous to yeast and mammalian cAMP-dependent protein kinase catalytic subunits. In addition to suppressing loss of CDC25 function, multicopy plasmids containing SCH9 suppress the growth defects of strains lacking the RAS genes, the CYR1 gene, which encodes adenylyl cyclase, and the TPK genes, which encode the cAMP-dependent protein kinase catalytic subunits. Cells lacking SCH9 grow slowly and have a prolonged G1 phase of the cell cycle. This defect is suppressed by activation of the cAMP effector pathway. We propose that SCH9 encodes a protein kinase that is part of a growth control pathway which is at least partially redundant with the cAMP pathway.
通过其对cdc25ts突变的互补能力,从酿酒酵母中分离出一个新基因SCH9。序列分析表明,它编码一种90,000道尔顿的蛋白质,其羧基末端结构域与酵母和哺乳动物的cAMP依赖性蛋白激酶催化亚基同源。除了抑制CDC25功能丧失外,含有SCH9的多拷贝质粒还能抑制缺乏RAS基因、编码腺苷酸环化酶的CYR1基因以及编码cAMP依赖性蛋白激酶催化亚基的TPK基因的菌株的生长缺陷。缺乏SCH9的细胞生长缓慢,细胞周期的G1期延长。cAMP效应途径的激活可抑制这一缺陷。我们提出,SCH9编码一种蛋白激酶,它是生长控制途径的一部分,该途径至少部分与cAMP途径冗余。