de la Fuente N, Portillo F
Instituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), Arturo Duperier 4, E-28029, Madrid, Spain.
Biochim Biophys Acta. 2000 Dec 20;1509(1-2):189-94. doi: 10.1016/s0005-2736(00)00293-5.
Glucose triggers transcriptional and post-transcriptional mechanisms that increase the amount and the activity of Saccharomyces cerevisiae plasma membrane H(+)-ATPase. In a previous study, we found that a mutation in the Rsp5 ubiquitin-protein ligase enzyme affected the post-transcriptional activation of the enzyme by glucose. Mutations at the RSP5 locus alter the glucose-triggered K(m) decrease. In a genetic screening for multicopy suppressors of the rsp5 mutation, we identified the WSC2/YNL283c gene. Deletion of the WSC2 gene disturbs ATPase activation by glucose, abolishing the K(m) decrease that occurs during this process. Wsc2 is a component of the PKC1-MPK1 mitogen-activated protein kinase (MAPK) signaling pathway that controls the cell wall integrity. Deletion of the MPK1/SLT2 gene disturbs the glucose-triggered K(m) decrease in ATPase.
葡萄糖触发转录和转录后机制,增加酿酒酵母质膜H(+)-ATP酶的量和活性。在先前的研究中,我们发现Rsp5泛素蛋白连接酶的突变影响了葡萄糖对该酶的转录后激活。RSP5位点的突变改变了葡萄糖触发的K(m)降低。在对rsp5突变的多拷贝抑制子进行的遗传筛选中,我们鉴定出了WSC2/YNL283c基因。WSC2基因的缺失扰乱了葡萄糖对ATP酶的激活,消除了在此过程中发生的K(m)降低。Wsc2是PKC1-MPK1丝裂原活化蛋白激酶(MAPK)信号通路的一个组成部分,该信号通路控制细胞壁完整性。MPK1/SLT2基因的缺失扰乱了葡萄糖触发的ATP酶K(m)降低。