In this study we analyze the participation of the PKC1-MAPK cell integrity pathway in cellular re- sponses to oxidative stress in Saccharomyces cerevisiae. Evidence is presented demonstrating that only Pkc1 and the upstream elements of the cell integrity pathway are essential for cell survival upon treatment with two oxidizing agents, diamide and hydrogen peroxide. Mtl1 is characterized for the first time as a cell-wall sensor of oxidative stress. We also show that the actin cytoskele- ton is a cellular target for oxidative stress. Both diamide and hydrogen peroxide provoke a marked depolariza- tion of the actin cytoskeleton, being Mtl1, Rom2 and Pkc1 functions all required to restore the correct actin organization. Diamide induces the formation of disul- fide bonds in newly secreted cell-wall proteins. This mainly provokes structural changes in the cell outer layer, which activate the PKC1-MAPK pathway and hence the protein kinase Slt2. Our results led us to the conclusion that Pkc1 activity is required to overcome the effects of oxidative stress by: (i) enhancing the ma- chinery required to repair the altered cell wall and (ii) restoring actin cytoskeleton polarity by promoting actin cable formation.