The HOG MAPK pathway and yeast stress responses: Roles in oxidative stress and heat shock

[摘要] The HOG MAP kinase pathway in the budding yeast Saccharomyces cerevisiae senses and responds to high osmolarity. Here we demonstrated that HOG pathway mutants are hypersensitive to K1 killer toxin, which implies certain defects in their cell wall. Overexpression of the PBS2 gene leads to enhanced resistance to K1 killer toxin. Treating yeast cells with a pore-forming antifungal agent, amphotericin B, lowers the cellular turgor pressure. More importantly, amphotericin B treatment leads to activation of the HOG pathway, supporting the hypothesis that loss of turgor pressure activates the HOG pathway. Deficiencies in the HOG pathway also cause hypersensitivity to hydrogen peroxide and the superoxide-generating drug plumbagin. Hydrogen peroxide, menadione and plumbagin all activate the HOG pathway. The HOG pathway acts parallel to Skn7p and Yap1p in oxidative stress response, evidenced by the additive effect of hog1Delta, skn7Delta and yap1Delta on hydrogen peroxide sensitivity. Both ssn6Delta and sko1Delta suppress hog1Delta mutant sensitivity to oxidants. Oxidative stress induces transcription of HSP12 and HSP26. The HOG pathway regulates HSP12 transcription in this response. Msn2p and Msn4p are important for the oxidative stress-induced transcription of HSP12 and HSP26. The HOG pathway is also involved in heat shock response. Cells lacking the HOG1 gene are hypersensitive to heat stress. A temperature shift from 25°C to 37°C activates the HOG pathway. Such an increase in temperature also induces transcription of HSP12 and HSP26. The HOG pathway regulates HSP12 transcription in the heat shock response. Msn2p and Msn4p are important for the heat shock-induced transcription of HSP12 and HSP26.

[发布机构] Rice University