A key player in the S. cerevisiae osmotic response pathway, the p38 mitogen-activated protein kinase (MAPK) Hog1, is activated not only in response to osmotic stress, but in other stress responses as well. Hog1 seems to activate different gene expression programs in high salt stress, cell wall damage and osmotic stress by targeting different transcription factors. In high salt (KCl), Hog1 activates transcription factors Msn 2/4, Sko1 and Hot1, while in high glucose, Hog1 only activates Sko1 and Hot1 (Pascual-Ahuir et al, 2001, O'Rourke et al, 2004). The cell wall damage response differs slightly from the high osmolarity responses because relatively little Hog1 is transported into the nucleus, and both Slt2 (Mpk1) and Hog1 activate the transcription factor Rlm1 (Alonso-Monge et al, 2001, Boorsma et al, 2004, Bermejo et al, 2008). The roles of Hog1 and Slt2 in high salt and cell wall damage responses have been explored, but the exact regulatory roles of Hog1, Slt2 and Rlm1 in the cellular responses to heat stress and oxidative stress have yet to be determined.
My project is an explorative study of signal integration in yeast, and I will start by asking whether the HOG MAPK pathway kinase Hog1 plays a role in the oxidative stress response. I will use DNA microarrays to analyze which transcription factors (Msn 2/4, Sko1/Hot1, Rlm1) are activated by MAPKs (Slt2 or Hog1) in untreated and oxidant treated cells.
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