Regulation of cell cycle progression by Swe1p and Hog1p following hypertonic stress.
Regulation of cell cycle progression by Swe1p and Hog1p following hypertonic stress.
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高渗应激后 Swe1p 和 Hog1p 对细胞周期进程的调节。
DOI：
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发表时间：
2001
影响因子：
3.3
通讯作者：
M. Gustin
中科院分区：
文献类型：
--
作者：
M. Alexander;M. Tyers;M. Perret;B. M. Craig;K. Fang;M. Gustin
酵母细胞暴露于外部渗透压的增加诱导暂时的生长停滞。从这种压力的恢复是介导的细胞内甘油的积累和转录的几个压力反应基因。增加的外部渗透压导致1N和2N细胞的瞬时积累和S期细胞的伴随消耗。高渗应激触发G2期细胞的细胞周期延迟，这似乎与在早期S期细胞中起作用的形态发生检查点不同。高渗应激导致CLB2 mRNA的减少、Cdc28p的磷酸化和Clb2p-Cdc28p激酶活性的抑制，而Clb2蛋白水平不受影响。与形态发生检查点一样，渗透胁迫诱导的G2延迟依赖于激酶Swe1p，但与Clb2p-Cdc28p激酶活性的抑制并不紧密相关。因此，SWE1的缺失不能阻止高渗应激诱导的Clb2p-Cdc28p激酶活性抑制。Cdc28p（Y19）上的Swe1p磷酸化位点的突变不能完全消除Swe1p依赖的细胞周期延迟，这表明Swe1p可能具有独立于Cdc28p磷酸化的功能。相反，有丝分裂原活化蛋白激酶HOG 1的缺失确实可以阻止高渗应激对Clb 2p-Cdc 28 p的抑制，但不会阻止Cdc 28 p的磷酸化或缓解细胞周期延迟。然而，在缺乏Swe1p的细胞中，Hog1p确实有助于高渗应激后的适当核分离。这些结果表明，高渗应激诱导的细胞周期延迟在G2期，介导的一种新的方式Swe1p与Hog1p的合作。
Exposure of yeast cells to an increase in external osmolarity induces a temporary growth arrest. Recovery from this stress is mediated by the accumulation of intracellular glycerol and the transcription of several stress response genes. Increased external osmolarity causes a transient accumulation of 1N and 2N cells and a concomitant depletion of S phase cells. Hypertonic stress triggers a cell cycle delay in G2 phase cells that appears distinct from the morphogenesis checkpoint, which operates in early S phase cells. Hypertonic stress causes a decrease in CLB2 mRNA, phosphorylation of Cdc28p, and inhibition of Clb2p-Cdc28p kinase activity, whereas Clb2 protein levels are unaffected. Like the morphogenesis checkpoint, the osmotic stress-induced G2 delay is dependent upon the kinase Swe1p, but is not tightly correlated with inhibition of Clb2p-Cdc28p kinase activity. Thus, deletion of SWE1 does not prevent the hypertonic stress-induced inhibition of Clb2p-Cdc28p kinase activity. Mutation of the Swe1p phosphorylation site on Cdc28p (Y19) does not fully eliminate the Swe1p-dependent cell cycle delay, suggesting that Swe1p may have functions independent of Cdc28p phosphorylation. Conversely, deletion of the mitogen-activated protein kinase HOG1 does prevent Clb2p-Cdc28p inhibition by hypertonic stress, but does not block Cdc28p phosphorylation or alleviate the cell cycle delay. However, Hog1p does contribute to proper nuclear segregation after hypertonic stress in cells that lack Swe1p. These results suggest a hypertonic stress-induced cell cycle delay in G2 phase that is mediated in a novel way by Swe1p in cooperation with Hog1p.
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影响因子：
3.3
作者：
Sia, RAL;Herald, HA;Lew, DJ
通讯作者：
Lew, DJ
影响因子：
10.5
作者：
WEINERT, TA;KISER, GL;HARTWELL, LH
通讯作者：
HARTWELL, LH
影响因子：
11.4
作者：
TYERS, M;TOKIWA, G;FUTCHER, B
通讯作者：
FUTCHER, B
影响因子：
10.5
作者：
Barral, Y;Parra, M;Snyder, M
通讯作者：
Snyder, M
影响因子：
11.4
作者：
BOOHER, RN;DESHAIES, RJ;KIRSCHNER, MW
通讯作者：
KIRSCHNER, MW