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MBC in Press, published online ahead of print June 27, 2003
Mol. Biol. Cell 10.1091/mbc.E03-02-0113

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Submitted on February 26, 2003
Revised on May 27, 2003
Accepted on June 6, 2003

MAP kinase Stimulation of Ca2+ Signaling is Required for Survival of Endoplasmic Reticulum Stress in Yeast

Myriam Bonilla1 and Kyle W. Cunningham1*

1 Department of Biology, Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218, USA

* Corresponding author. E-mail address: kwc{at}jhu.edu.

ER stress in the budding yeast S. cerevisiae triggers Ca2+ influx through a plasma membrane channel composed of Cch1 and Mid1. This response activates calcineurin, which helps to prevent cell death during multiple forms of ER stress including the response to azole-class antifungal drugs. Here we show that ER stress activates the cell integrity MAP kinase cascade in yeast and that the activation of Pkc1 and Mpk1 is necessary for stimulation of the Cch1-Mid1 Ca2+ channel independent of many known targets of Mpk1 (Rlm1, Swi4, Swi6, Mih1, Hsl1, and Swe1). ER stress generated in response to miconazole, tunicamycin, or other inhibitors also triggered a transient G2/M arrest that depended upon the Swe1 protein kinase. Calcineurin played little role in the Swe1-dependent cell cycle arrest and Swe1 had little effect on calcineurin-dependent avoidance of cell death. These findings help to clarify the interactions between Mpk1, calcineurin, and Swe1 and suggest that the calcium cell survival pathway promotes drug resistance independent of both the unfolded protein response and the G2/M cell cycle checkpoint.




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