The checkpoint kinase Hsl1p is activated by Elm1p-dependent phosphorylation.


Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Szkotnicki, L; Crutchley, JM; Zyla, TR; Bardes, ESG; Lew, DJ

Published Date

  • November 2008

Published In

Volume / Issue

  • 19 / 11

Start / End Page

  • 4675 - 4686

PubMed ID

  • 18768748

Pubmed Central ID

  • 18768748

Electronic International Standard Serial Number (EISSN)

  • 1939-4586

Digital Object Identifier (DOI)

  • 10.1091/mbc.e08-06-0663


  • eng

Conference Location

  • United States