Regulation of cell cycle and stress responses to hydrostatic pressure in fission yeast
Regulation of cell cycle and stress responses to hydrostatic pressure in fission yeast
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DOI：
10.1091/mbc.e06-12-1141
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发表时间：
2007-10-01
影响因子：
3.3
通讯作者：
Humphrey, Timothy C.
中科院分区：
文献类型：
--
作者：
George, Vinoj T.;Brooks, Gavin;Humphrey, Timothy C.
以裂殖酵母裂殖酵母为模型系统，研究了细胞对静水压力的反应。暴露于亚致死水平的静水压力导致G2期细胞周期延迟。这种延迟是由Cdc 2酪氨酸-15（Y-15）磷酸化引起的，并且通过同时破坏Cdc 2激酶调节剂Cdc 25和Wee 1来消除。然而，细胞周期延迟是独立的DNA损伤，胞质分裂，和细胞大小的检查点，这表明一种新的机制Cdc 2-Y15磷酸化响应静水压力。Spc 1/Sty 1丝裂原活化蛋白（MAP）激酶是真核细胞应激活化的p38丝裂原活化蛋白（MAP）激酶家族的一个保守成员，在压力应激后迅速活化，并在这些条件下为细胞周期恢复所必需，部分通过促进丝氨酸402上的波罗激酶（Plo 1）磷酸化。此外，Spc 1 MAP激酶途径通过bZip转录因子Atf 1在静水压力应激下维持细胞活力中发挥关键作用。进一步的分析表明，预应力细胞与热增加耐压性，这表明这些应力响应之间的适应性串扰。这些发现提供了新的见解真核生物的稳态暴露后的压力。
We have investigated the cellular responses to hydrostatic pressure by using the fission yeast Schizosaccharomyces pombe as a model system. Exposure to sublethal levels of hydrostatic pressure resulted in G2 cell cycle delay. This delay resulted from Cdc2 tyrosine-15 (Y-15) phosphorylation, and it was abrogated by simultaneous disruption of the Cdc2 kinase regulators Cdc25 and Wee1. However, cell cycle delay was independent of the DNA damage, cytokinesis, and cell size checkpoints, suggesting a novel mechanism of Cdc2-Y15 phosphorylation in response to hydrostatic pressure. Spc1/Sty1 mitogen-activated protein (MAP) kinase, a conserved member of the eukaryotic stress-activated p38, mitogen-activated protein (MAP) kinase family, was rapidly activated after pressure stress, and it was required for cell cycle recovery under these conditions, in part through promoting polo kinase (Plo1) phosphorylation on serine 402. Moreover, the Spc1 MAP kinase pathway played a key role in maintaining cell viability under hydrostatic pressure stress through the bZip transcription factor, Atf1. Further analysis revealed that prestressing cells with heat increased barotolerance, suggesting adaptational cross-talk between these stress responses. These findings provide new insight into eukaryotic homeostasis after exposure to pressure stress.