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Originally published as MBC in Press, 10.1091/mbc.E08-06-0663 on September 3, 2008

Vol. 19, Issue 11, 4675-4686, November 2008

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The Checkpoint Kinase Hsl1p Is Activated by Elm1p-dependent Phosphorylation

Lee Szkotnicki, John M. Crutchley, Trevin R. Zyla, Elaine S.G. Bardes, and Daniel J. Lew

Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710

Submitted July 1, 2008; Revised August 19, 2008; Accepted August 21, 2008
Monitoring Editor: Mark J. Solomon

Saccharomyces cerevisiae cells growing in the outdoor environment must adapt to sudden changes in temperature and other variables. Many such changes trigger stress responses that delay bud emergence until the cells can adapt. In such circumstances, the morphogenesis checkpoint delays mitosis until a bud has been formed. Mitotic delay is due to the Wee1 family mitotic inhibitor Swe1p, whose degradation is linked to bud emergence by the checkpoint kinase Hsl1p. Hsl1p is concentrated at the mother-bud neck through association with septin filaments, and it was reported that Hsl1p activation involved relief of autoinhibition in response to septin interaction. Here we challenge the previous identification of an autoinhibitory domain and show instead that Hsl1p activation involves the phosphorylation of threonine 273, promoted by the septin-associated kinase Elm1p. We identified elm1 mutants in a screen for defects in Swe1p degradation and show that a phosphomimic T273E mutation in HSL1 bypasses the need for Elm1p in this pathway.

This was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E08-06-0663) on September 3, 2008.

Address correspondence to: Daniel J. Lew (daniel.lew{at}duke.edu)




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