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Regulation of cell cycle and stress responses to hydrostatic pressure in fission yeast

机译：调节裂变酵母中细胞周期和应激对静水压力的响应

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摘要

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.
机译：我们已经通过使用裂殖酵母粟酒裂殖酵母（Schizosaccharomyces pombe）作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细胞周期延迟。这种延迟是由于Cdc2酪氨酸15（Y-15）磷酸化引起的，并且由于同时破坏Cdc2激酶调节剂Cdc25和Wee1而被取消。但是，细胞周期延迟与DNA损伤，胞质分裂和细胞大小检查点无关，这表明Cdc2-Y15磷酸化响应静水压力的新机制。 Spc1 / Sty1丝裂原激活蛋白（MAP）激酶是真核生物应力激活p38的保守成员，丝裂原激活蛋白（MAP）激酶家族，在压力胁迫下迅速被激活，在这些条件下细胞周期恢复是必需的这种情况，部分是通过促进丝氨酸402上的polo激酶（Plo1）磷酸化来实现的。此外，Spc1 MAP激酶途径在通过bZip转录因子Atf1静水压胁迫下维持细胞活力中起着关键作用。进一步的分析表明，带有热的预应力细胞增加了耐压性，表明这些应激反应之间存在适应性串扰。这些发现为接触压力后的真核生物稳态提供了新的见解。

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