State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China.
The Key Laboratory of Industrial Biotechnology, Ministry of Education, Jiangnan University, Wuxi, Jiangsu, China.
Appl Environ Microbiol. 2019 Mar 6;85(6). doi: 10.1128/AEM.02822-18. Print 2019 Mar 15.
Under stress conditions, Hog1 is required for cell survival through transiently phosphorylating downstream targets and reprogramming gene expression. Here, we report that Hog1 (Hog1) interacts with and phosphorylates Rds2, a zinc cluster transcription factor, in response to osmotic stress. Additionally, we found that deletion of led to decreases in cell growth and cell survival by 23.4% and 39.6%, respectively, at 1.5 M NaCl, compared with levels of the wild-type strain. This is attributed to significant downregulation of the expression levels of glycerophospholipid metabolism genes. As a result, the content of total glycerophospholipid decreased by 30.3%. Membrane integrity also decreased 47.6% in the Δ strain at 1.5 M NaCl. In contrast, overexpression of increased the cell growth and cell survival by 10.2% and 6.3%, respectively, owing to a significant increase in the total glycerophospholipid content and increased membrane integrity by 27.2% and 12.1%, respectively, at 1.5 M NaCl, compared with levels for the wild-type strain. However, a strain in which the gene encodes the replacement of Ser64 and Thr97 residues with alanines ( ), harboring a Rds2 protein that was not phosphorylated by Hog1, failed to promote glycerophospholipid metabolism and membrane integrity at 1.5 M NaCl. Thus, the above results demonstrate that Hog1-mediated Rds2 phosphorylation enhanced glycerophospholipid composition and membrane integrity to resist osmotic stress in This study explored the role of Hog1-mediated Rds2 phosphorylation in response to osmotic stress in Hog1 interacts with and phosphorylates Rds2, a zinc cluster transcription factor, under osmotic stress. Phosphorylated Rds2 plays an important role in increasing glycerophospholipid composition and membrane integrity, thereby enhancing cell growth and survival.
在应激条件下，Hog1 通过暂时磷酸化下游靶标和重新编程基因表达来促进细胞存活。在这里，我们报告 Hog1（Hog1）与锌簇转录因子 Rds2 相互作用并磷酸化 Rds2，以响应渗透胁迫。此外，我们发现缺失导致细胞生长和细胞存活分别下降 23.4%和 39.6%，在 1.5 M NaCl 时，与野生型菌株相比。这归因于甘油磷脂代谢基因表达水平的显著下调。结果，总甘油磷脂含量下降了 30.3%。在 1.5 M NaCl 时，Δ 菌株的膜完整性也下降了 47.6%。相比之下，由于总甘油磷脂含量显著增加，膜完整性分别增加了 27.2%和 12.1%，在 1.5 M NaCl 时，过表达增加了细胞生长和细胞存活分别为 10.2%和 6.3%，与野生型菌株相比。然而，编码 Ser64 和 Thr97 残基被丙氨酸取代的 基因（ ）的菌株，携带不能被 Hog1 磷酸化的 Rds2 蛋白，不能促进甘油磷脂代谢和膜完整性在 1.5 M NaCl 下。因此，上述结果表明，Hog1 介导的 Rds2 磷酸化增强了甘油磷脂组成和膜完整性，以抵抗渗透压胁迫。本研究探讨了 Hog1 介导的 Rds2 磷酸化在应对渗透压胁迫中的作用 Hog1 与锌簇转录因子 Rds2 相互作用并磷酸化 Rds2，以响应渗透胁迫。磷酸化的 Rds2 在增加甘油磷脂组成和膜完整性方面发挥重要作用，从而增强细胞生长和存活。
