Pkc1 and the upstream elements of the cell integrity pathway in Saccharomyces cerevisiae, Rom2 and Mtl1, are required for cellular responses to oxidative stress

Vilella Mitjana, Felipe; Herrero Perpiñán, Enrique; Torres Rosell, Jordi; Torre Ruiz, M. A. de la

doi:https://doi.org/10.1074/jbc.M411062200

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Issue date

2005

Author

Vilella Mitjana, Felipe

Herrero Perpiñán, Enrique

Torres Rosell, Jordi

Torre Ruiz, M. A. de la

Suggested citation

Vilella Mitjana, Felipe; Herrero Perpiñán, Enrique; Torres Rosell, Jordi; Torre Ruiz, M. A. de la; . (2005) . Pkc1 and the upstream elements of the cell integrity pathway in Saccharomyces cerevisiae, Rom2 and Mtl1, are required for cellular responses to oxidative stress. The Journal of Biological Chemistry, 2005, vol. 280, núm 10, p. 9149-9159. https://doi.org/10.1074/jbc.M411062200.

Abstract

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.

URI

http://hdl.handle.net/10459.1/48444

DOI

https://doi.org/10.1074/jbc.M411062200

Is part of

The Journal of Biological Chemistry, 2005, vol. 280, núm 10, p. 9149-9159