Modulation of yeast Sln1 kinase activity by the Ccw12 cell wall protein
Modulation of yeast Sln1 kinase activity by the Ccw12 cell wall protein
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DOI：
10.1074/jbc.m706877200
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发表时间：
2008-01-25
影响因子：
4.8
通讯作者：
Fassler, Jan S.
中科院分区：
文献类型：
--
作者：
Narang, Sandhya S.;Malone, Cheryl L.;Fassler, Jan S.
酵母Sln1p传感激酶是一种渗透传感器，参与调节高渗透压甘油丝裂原激活的蛋白激酶级联反应。Sln1激酶活性的下调发生在高渗条件下，导致Hog1p丝裂原活化蛋白激酶磷酸化和渗透应激反应基因表达增加。导致激酶上调的条件包括甘油通道突变体fps1中甘油滞留引起的渗透失衡(Tao， W., Deschenes， R. J., and Fassler， J. S. (1999) J. Biol。化学，274,360 -367)。Sln1p激酶活性对肿胀有反应的假设最初是由缺乏Fps1p的突变体中Sln1p激酶活性增加而提出的，在这种突变体中甘油积累导致水分摄取。与肿胀假说一致的是，观察到用制霉素（一种增加膜通透性并导致细胞收缩的药物）治疗细胞引起的肿胀减少，降低了Sln1p激酶活性(Tao， W., Deschenes， R. J., and Fassler， J. S. (1999) J. Biol。化学学报，274,360 -367；Reiser， V., Raitt, d.c, and Saito， H. (2003) J.细胞生物学，161,1035-1040)。在细胞壁基因CCW12作为Sln1p活性决定因素的鉴定和表征的背景下，我们重新审视了膨胀假说。这一分析结果表明，质膜定位Sln1p的活性受到特定外细胞壁蛋白存在与否的影响，并且这种影响与肿胀无关。
The yeast Sln1p sensor kinase is best known as an osmosensor involved in the regulation of the hyperosmolarity glycerol mitogen-activated protein kinase cascade. Down-regulation of Sln1 kinase activity occurs under hypertonic conditions and leads to phosphorylation of the Hog1p mitogen-activated protein kinase and increased osmotic stress-response gene expression. Conditions leading to kinase up-regulation include osmotic imbalance caused by glycerol retention in the glycerol channel mutant, fps1 (Tao, W., Deschenes, R. J., and Fassler, J. S. (1999) J. Biol. Chem. 274, 360-367). The hypothesis that Sln1p kinase activity is responsive to turgor was first suggested by the increased Sln1p kinase activity in mutants lacking Fps1p in which glycerol accumulation leads to water uptake. Also consistent with the turgor hypothesis is the observation that reduced turgor caused by treatment of cells with nystatin, a drug that increases membrane permeability and causes cell shrinkage, reduced Sln1p kinase activity (Tao, W., Deschenes, R. J., and Fassler, J. S. (1999) J. Biol. Chem. 274, 360-367; Reiser, V., Raitt, D. C., and Saito, H. (2003) J. Cell Biol. 161, 1035-1040). The turgor hypothesis is revisited here in the context of the identification and characterization of the cell wall gene, CCW12, as a determinant of Sln1p activity. Results of this analysis suggest that the activity of the plasma membrane localized Sln1p is affected by the presence or absence of specific outer cell wall proteins and that this effect is independent of turgor.