Cell wall perturbation in yeast results in dual phosphorylation of the Slt2/Mpk1 MAP kinase and in an Slt2-mediated increase in FKS2-lacZ expression, glucanase resistance and thermotolerance
Cell wall perturbation in yeast results in dual phosphorylation of the Slt2/Mpk1 MAP kinase and in an Slt2-mediated increase in FKS2-lacZ expression, glucanase resistance and thermotolerance
复制标题
DOI：
10.1099/00221287-146-9-2121
复制
发表时间：
2000-09-01
期刊：
影响因子：
2.8
通讯作者：
Klis, FM
中科院分区：
文献类型：
--
作者：
de Nobel, H;Ruiz, C;Klis, FM
蛋白激酶C（PKC 1）途径对于维持酵母细胞的完整性至关重要。这里显示，各种形式的细胞壁损伤导致下游MAP激酶Slt 2/Mpk 1的激活。几种细胞壁突变体显示FKS 2-lacZ表达增强，这是Slt 2激活的已知输出。在细胞壁扰动剂Calcofluor白色和酵母菌酶存在下生长的野生型细胞获得了类似的反应。FKS 2-lacZ的上调响应于亚致死浓度的这些药剂完全在双苏氨酸和酪氨酸磷酸化的Slt 2。Slt 2磷酸化和FKS 2-lacZ诱导可以通过向质膜提供渗透支持来在很大程度上防止。有趣的是，响应于细胞壁损伤的Slt 2磷酸化需要假定的质膜定位传感器Mid 2，而不是Hcs 77/Wsc 1。最后，细胞壁扰动引起细胞对葡聚糖酶消化和热休克的抗性增加。这些反应依赖于Slt 2的存在。这些结果表明，细胞壁的弱化激活了Slt 2/Mpk 1 MAP激酶途径，并导致细胞壁的代偿性变化。
The protein kinase C (PKC1) pathway is essential for maintaining cell integrity in yeast. Here it is shown that various forms of cell wall damage result in activation of the downstream MAP kinase Slt2/Mpk1. Several cell wall mutants displayed enhanced FKS2-lacZ expression, a known output of Slt2 activation. A similar response was obtained with wild-type cells grown in the presence of the cell wall perturbants Calcofluor white and Zymolyase. Upregulation of FKS2-lacZ in response to sublethal concentrations of these agents fully in dual threonine and tyrosine phosphorylation of Slt2. Both Slt2 phosphorylation and FKS2-lacZ induction could be largely prevented by providing osmotic support to the plasma membrane. Interestingly, Slt2 phosphorylation in response to cell wall damage required the putative plasmamembrane-located sensor Mid2 but not Hcs77/Wsc1. Finally, cell wall perturbation gave rise to cells with increased resistance to glucanase digestion and heat shock. These responses depended on the presence of Slt2. These results indicate that weakening of the cell wall activates the Slt2/Mpk1 MAP kinase pathway and results in compensatory changes in the cell wall.