Abstract

DNA damage is a harmful and unavoidable stress frequently encountered by living organisms. It is crucial for organisms to have elaborated mechanisms in response to DNA damage, and a thorough understanding of these mechanisms and their regulation is very important. Hog1 is a stress‐activated protein kinase in Saccharomyces cerevisiae, which responds to osmolarity changes as well as various other stressors. Recently, we found that Hog1 can be activated by DNA damage agent, and the activation is primarily mediated by the Sln1 branch of the HOG pathway. Interestingly, we observed that DNA damage agent‐induced activation of Hog1 is substantially elevated when treated with cycloheximide, a protein synthesis inhibitor, suggesting the existence of a mechanism that keeps the extent of Hog1 activation in check. Notably, the cycloheximide effect is diminished in several phosphatase deletion mutants, suggesting a profound involvement of phosphatase in this process. The detailed characterization of the role of phosphatase in regulating DNA damage‐induced Hog1 activation is currently underway.

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