Mcs4 mitotic catastrophe suppressor regulates the fission yeast cell cycle through the Wik1-Wis1-Spc1 kinase cascade.
Mcs4 mitotic catastrophe suppressor regulates the fission yeast cell cycle through the Wik1-Wis1-Spc1 kinase cascade.
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Mcs4 有丝分裂突变抑制因子通过 Wik1-Wis1-Spc1 激酶级联调节裂殖酵母细胞周期。
DOI：
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发表时间：
1997
影响因子：
3.3
通讯作者：
P. Russell
中科院分区：
文献类型：
--
作者：
K. Shiozaki;M. Shiozaki;P. Russell
裂殖酵母Spc 1是应力活化蛋白激酶家族的成员，应力活化蛋白激酶家族是丝裂原活化蛋白激酶（MAPK）的进化保守亚家族。Spc 1由MAPK激酶同源物Wis 1激活，并由Pyp 1和Pyp 2酪氨酸磷酸酶负调控。spc 1+和wis 1+基因的突变导致G2细胞周期延迟，在应激期间加剧。在这里，我们描述了两个上游调节Wis 1-Spc 1级联。wik 1+（Wis 1激酶）通过其与芽殖酵母SSK 2的同源性而被鉴定，SSK 2编码调节HOG 1 β传感途径的MAPKK激酶。Delta wik 1细胞在应激诱导的Spc 1激活中受损，并显示G2细胞周期延迟和对细胞周期敏感的生长。此外，组成型活性形式的Wik 1的过量产生以wis 1（+）依赖的方式诱导Spc 1的过度激活，表明Wik 1通过激活Wis 1调节Spc 1。mcs 4+突变（有丝分裂灾难抑制因子）最初是作为cdc 2 - 3 w wee 1 -50双突变体的有丝分裂灾难表型的抑制因子分离出来的。我们已经发现，MCS 4-细胞在响应于各种形式的应激的Spc 1的激活方面有缺陷。上位性分析将Mcs 4-置于Spc 1激活级联中Wik 1的上游。这些结果表明，Mcs 4是多个环境信号的传感器系统的一部分，该系统通过调节Wik 1-Wis 1-Spc 1激酶级联来调节进入有丝分裂的时间。感应系统的失活延迟了cdc 2 - 3 w wee 1 -50细胞有丝分裂的开始并挽救了致命的过早有丝分裂。
Spc1 in Schizosaccharomyces pombe is a member of the stress-activated protein kinase family, an evolutionary conserved subfamily of mitogen-activated protein kinases (MAPKs). Spc1 is activated by a MAPK kinase homologue, Wis1, and negatively regulated by Pyp1 and Pyp2 tyrosine phosphatases. Mutations in the spc1+ and wis1+ genes cause a G2 cell cycle delay that is exacerbated during stress. Herein, we describe two upstream regulators of the Wis1-Spc1 cascade. wik1+ (Wis1 kinase) was identified from its homology to budding yeast SSK2, which encodes a MAPKK kinase that regulates the HOG1 osmosensing pathway. Delta wik1 cells are impaired in stress-induced activation of Spc1 and show a G2 cell cycle delay and osmosensitive growth. Moreover, overproduction of a constitutively active form of Wik1 induces hyperactivation of Spc1 in wis1(+)-dependent manner, suggesting that Wik1 regulates Spc1 through activation of Wis1. A mutation of mcs4+ (mitotic catastrophe suppressor) was originally isolated as a suppressor of the mitotic catastrophe phenotype of a cdc2-3w wee1-50 double mutant. We have found that mcs4- cells are defective at activation of Spc1 in response to various forms of stress. Epistasis analysis has placed Mcs4-upstream of Wik1 in the Spc1 activation cascade. These results indicate that Mcs4 is part of a sensor system for multiple environmental signals that modulates the timing of entry into mitosis by regulating the Wik1-Wis1-Spc1 kinase cascade. Inactivation of the sensor system delays the onset of mitosis and rescues lethal premature mitosis in cdc2-3w wee1-50 cells.
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影响因子：
56.9
作者：
HAN, J;LEE, JD;ULEVITCH, RJ
通讯作者：
ULEVITCH, RJ
影响因子：
3.3
作者：
Lisa Molz;R. Booher;’. PaulYoung;David Beach
通讯作者：
Lisa Molz;R. Booher;’. PaulYoung;David Beach
裂殖酵母 mcs2 细胞周期蛋白及其相关蛋白激酶活性的表征。
DOI：
10.1002/j.1460-2075.1993.tb05817.x
发表时间：
1993
期刊：
The EMBO journal
影响因子：
--
作者：
Molz,L;Beach,D
通讯作者：
Beach,D
裂殖酵母基因编码具有蛋白质酪氨酸磷酸酶特征的蛋白质。
DOI：
10.1073/pnas.88.8.3455
发表时间：
1991
影响因子：
11.1
作者：
Ottilie,S;Chernoff,J;Hannig,G;Hoffman,CS;Erikson,RL
通讯作者：
Erikson,RL