Proper protein glycosylation promotes mitogen-activated protein kinase signal fidelity.
Proper protein glycosylation promotes mitogen-activated protein kinase signal fidelity.
复制标题
DOI：
10.1021/bi3009483
复制
发表时间：
2013-01-08
期刊：
影响因子：
2.9
通讯作者：
Dohlman HG
中科院分区：
文献类型：
--
作者：
Lien EC;Nagiec MJ;Dohlman HG
细胞对变化的环境条件的感知和适当响应的能力通常由采用促分裂原活化蛋白激酶（MAPK）的信号转导途径介导。在酿酒酵母中，高渗甘油（HOG）和丝状生长（FG）途径分别在高渗胁迫和营养剥夺后被激活。HOG途径需要MAPK Hog 1，而FG途径使用MAPK Kss 1。我们对近5,000株基因缺失菌株进行了全面筛选，以寻找在HOG和FG途径之间表现出不适当串扰的突变体。我们鉴定了两种新的突变体mnn 10 Δ和mnn 11 Δ，它们允许在通常刺激Hog 1的条件下激活Kss 1。MNN 10和MNN 11编码甘露糖基转移酶，它们是高尔基体内N-糖基化机制的一部分;缺失任一基因都会导致具有较短甘露聚糖链的N-糖基化蛋白质。细胞表面粘蛋白Msb 2的缺失抑制了mnn 11 Δ表型，而Msb 2内单个糖基化位点的突变足以通过盐胁迫赋予Kss 1不适当的激活。这些发现揭示了确保MAPK信号保真度所需的N-糖基化机制的新成分。
The ability of cells to sense and respond appropriately to changing environmental conditions is often mediated by signal transduction pathways that employ mitogen-activated protein kinases (MAPKs). In the yeast Saccharomyces cerevisiae, the high osmolarity glycerol (HOG) and the filamentous growth (FG) pathways are activated following hyperosmotic stress and nutrient deprivation, respectively. Whereas the HOG pathway requires the MAPK Hog1, the FG pathway employs the MAPK Kss1. We conducted a comprehensive screen of nearly 5,000 gene deletion strains for mutants that exhibit inappropriate cross-talk between the HOG and FG pathways. We identified two novel mutants, mnn10Δ and mnn11Δ, that allow activation of Kss1 under conditions that normally stimulate Hog1. MNN10 and MNN11 encode mannosyltransferases that are part of the N-glycosylation machinery within the Golgi apparatus; deletion of either gene results in N-glycosylated proteins that have shorter mannan chains. Deletion of the cell surface mucin Msb2 suppressed the mnn11Δ phenotype, while mutation of a single glycosylation site within Msb2 was sufficient to confer inappropriate activation of Kss1 by salt stress. These findings reveal new components of the N-glycosylation machinery needed to ensure MAPK signaling fidelity.
登录
查看更多内容
影响因子：
64.5
作者：
Dennis JW;Nabi IR;Demetriou M
通讯作者：
Demetriou M
影响因子：
3.3
作者：
Hao N;Yildirim N;Nagiec MJ;Parnell SC;Errede B;Dohlman HG;Elston TC
通讯作者：
Elston TC
影响因子：
64.5
作者：
Chou, S;Huang, L;Liu, HP
通讯作者：
Liu, HP
影响因子：
3.2
作者：
Bartkeviciute, D;Sasnauskas, K
通讯作者：
Sasnauskas, K
影响因子：
9.2
作者：
Hao, Nan;Behar, Marcelo;Dohlman, Henrik G.
通讯作者：
Dohlman, Henrik G.