Abstract
The UV stress response in mammalian cells is characterized by transcriptional changes aimed at regulating cell growth, repair and survival. Previous studies have suggested that highly conserved mitogen-activated protein kinase (MAPK) pathways mediate UVinduced stress signalling. Here, we examined the role of the Hog-1 and Mpk-1 MAPKs in the Saccharomyces cerevisiae UV response. Deletion of both Hog-1 and Mpk-1 enhanced sensitivity to UVC-induced cell death. However, activation of these pathways by osmotic stress prior to irradiation failed to cross-protect wild type cells from death. A dosedependent upregulation of active Hog-1 was observed in response to UVC irradiation, but elevated expression caused by pre-treatment with hyper-osmotic medium correlated with a decrease in viability. We speculate that Hog-1, like its mammalian homologue, may also activate pro-apoptotic pathways when highly expressed.