Brewster J L, Gustin M C
Department of Biochemistry and Cell Biology, Rice University, Houston, TX 77251.
Yeast. 1994 Apr;10(4):425-39. doi: 10.1002/yea.320100402.
The yeast Saccharomyces cerevisiae has a genetic program for selecting and assembling a bud site on the cell cortex. Yeast cells confine their growth to the emerging bud, a process directed by cortical patches of actin filaments within the bud. We have investigated how cells regulate budding in response to osmotic stress, focusing on the role of the high osmolarity glycerol response (HOG) pathway in mediating this regulation. An increase in external osmolarity induces a growth arrest in which actin filaments are lost from the bud. This is followed by a recovery phase in which actin filaments return to their original locations and growth of the original bud resumes. After recovery from osmotic stress, haploid cells retain an axial pattern of bud site selection while diploids change their bipolar budding pattern to an increased bias for forming a bud on the opposite side of the cell from the previous bud site. Mutants lacking the mitogen-activated protein (MAP) kinase encoded by HOG1 or the MAP kinase kinase encoded by PBS2 (previously HOG4) show a similar growth arrest after osmotic stress. However, in the recovery phase, the mutant cells (a) do not restart growth of the original bud but rather start a new bud, (b) fail to restore actin filaments to the original bud but move them to the new one, and (c) show a more random budding pattern. These defects are elicited by an increase in osmolarity and not by other environmental stresses (e.g., heat shock or change in carbon source) that also cause a temporary growth arrest and shift in actin distribution. Thus, the HOG pathway is required for repositioning of the actin cytoskeleton and the normal spatial patterns of cell growth after recovery from osmotic stress.
酿酒酵母具有一套遗传程序，用于在细胞皮层上选择并组装出芽位点。酵母细胞将其生长限制在新出现的芽中，这一过程由芽内肌动蛋白丝的皮层斑块所引导。我们研究了细胞如何响应渗透压胁迫来调节出芽，重点关注高渗甘油应答（HOG）途径在介导这种调节中的作用。外部渗透压的增加会导致生长停滞，此时芽中的肌动蛋白丝会消失。随后是一个恢复阶段，在此阶段肌动蛋白丝回到其原始位置，原始芽的生长恢复。从渗透压胁迫中恢复后，单倍体细胞保留轴向出芽位点选择模式，而二倍体细胞则将其双极出芽模式改变为更倾向于在与先前芽位点相对的细胞另一侧形成芽。缺乏由HOG1编码的丝裂原活化蛋白（MAP）激酶或由PBS2（先前为HOG4）编码的MAP激酶激酶的突变体，在渗透压胁迫后表现出类似的生长停滞。然而，在恢复阶段，突变细胞（a）不会重新开始原始芽的生长，而是开始一个新的芽，（b）无法将肌动蛋白丝恢复到原始芽，而是将它们移动到新的芽，并且（c）表现出更随机的出芽模式。这些缺陷是由渗透压增加引起的，而不是由其他也会导致暂时生长停滞和肌动蛋白分布变化的环境胁迫（例如热休克或碳源变化）引起的。因此，HOG途径对于渗透压胁迫恢复后肌动蛋白细胞骨架的重新定位和细胞生长的正常空间模式是必需的。
