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MBC in Press, published online ahead of print May 3, 2006
Mol. Biol. Cell 10.1091/mbc.E05-12-1102

A more recent version of this article appeared on July 1, 2006
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Submitted on December 6, 2005
Revised on April 17, 2006
Accepted on April 21, 2006

The Stress-activated MAP Kinase Signaling Cascade Promotes Exit from Mitosis

Vladimír Reiser,* Katharine E. D’Aquino, Ly-Sha Ee, and Angelika Amon

Center for Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge MA 02139

Monitoring Editor: Orna Cohen-Fix

In budding yeast, a signaling network known as the Mitotic Exit Network (MEN) triggers exit from mitosis. We find that hypertonic stress allows MEN mutants to exit from mitosis in a manner dependent on the HOG MAP kinase cascade. The HOG pathway drives exit from mitosis in MEN mutants by promoting the activation of the MEN effector, the protein phosphatase Cdc14. Activation of Cdc14 depends on the FEAR network, a group of proteins that functions in parallel to the MEN to promote Cdc14 function. Notably, exit from mitosis is promoted by the signaling branch defined by the Sho1 osmosensing system, but not by the Sln1 osmosensor of the HOG pathway. Our results suggest that the stress MAP kinase pathway mobilizes programs to promote completion of the cell cycle and entry into G1 under unfavorable conditions.

*Present address: Merck & Co., One Merck Drive, Whitehouse Station, NJ 07065.

Address correspondence to: Angelika Amon (angelika{at}mit.edu)




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