The Win 1 Mitotic Regulator Is a Component of the Fission Yeast Stress-activated Sty 1 MAPK Pathway
The Win 1 Mitotic Regulator Is a Component of the Fission Yeast Stress-activated Sty 1 MAPK Pathway
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Win 1 有丝分裂调节器是裂变酵母应激激活的 Sty 1 MAPK 途径的一个组成部分
DOI：
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发表时间：
1998
期刊：
影响因子：
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通讯作者：
J. Millar
中科院分区：
文献类型：
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作者：
J. Shieh;M. Wilkinson;J. Millar
分裂酵母Sty1丝裂原活化蛋白激酶（MAPK）及其激活因子Wis1 MAP激酶激酶（MAPKK）在细胞周期控制、性分化起始和细胞应激保护中发挥着重要作用。与哺乳动物JNK/ SAPK和p38/CSBP1 MAPKs一样，Sty1被一系列环境损伤激活，包括渗透胁迫、过氧化氢、紫外线、甲萘醌、热休克和蛋白质合成抑制剂大霉素。我们最近确定了Wis1 MAPKK的两个上游调控因子，即Wak1 MAPKK和Mcs4响应调控因子。然而，缺乏Mcs4或Wak1的细胞能够在应激条件下增殖并进行性别分化，这表明有其他途径控制Wis1 MAPKK。我们现在表明，这些额外的信号信息至少部分是由Win1有丝分裂调节因子提供的。我们发现，在多种环境胁迫下，Wak1和Win1协同控制Sty1的激活，但在营养不良条件下，Wak1和Win1在Sty1的控制中发挥不同的作用。我们的研究结果表明，应激激活的Sty1 MAPK整合了来自多种信号通路的信息。
The fission yeast Sty1 mitogen-activated protein (MAP) kinase (MAPK) and its activator the Wis1 MAP kinase kinase (MAPKK) are required for cell cycle control, initiation of sexual differentiation, and protection against cellular stress. Like the mammalian JNK/ SAPK and p38/CSBP1 MAPKs, Sty1 is activated by a range of environmental insults including osmotic stress, hydrogen peroxide, UV light, menadione, heat shock, and the protein synthesis inhibitor anisomycin. We have recently identified two upstream regulators of the Wis1 MAPKK, namely the Wak1 MAPKKK and the Mcs4 response regulator. Cells lacking Mcs4 or Wak1, however, are able to proliferate under stressful conditions and undergo sexual differentiation, suggesting that additional pathway(s) control the Wis1 MAPKK. We now show that this additional signal information is provided, at least in part, by the Win1 mitotic regulator. We show that Wak1 and Win1 coordinately control activation of Sty1 in response to multiple environmental stresses, but that Wak1 and Win1 perform distinct roles in the control of Sty1 under poor nutritional conditions. Our results suggest that the stress-activated Sty1 MAPK integrates information from multiple signaling pathways.
影响因子：
56.9
作者：
HAN, J;LEE, JD;ULEVITCH, RJ
通讯作者：
ULEVITCH, RJ
影响因子：
56.9
作者：
Posas, F;Saito, H
通讯作者：
Saito, H