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Osmotic stress causes a G 1 cell cycle delay and downregulation of Cln3/Cdc28 activity in Saccharomyces cerevisiae
Author(s) -
Bellí Gemma,
Garí Eloi,
Aldea Martí,
Herrero Enrique
Publication year - 2001
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2001.02297.x
Subject(s) - saccharomyces cerevisiae , cyclin dependent kinase 1 , osmotic shock , cell cycle , downregulation and upregulation , biology , microbiology and biotechnology , cell cycle protein , cyclin , osmotic concentration , cell cycle checkpoint , biochemistry , cell , yeast , gene
Moderate hyperosmotic stress on Saccharomyces cerevisiae cells produces a temporary delay at the G 1 stage of the cell cycle. This is accompanied by transitory downregulation of CLN1 , CLN2 and CLB5 transcript levels, although not of CLN3 , which codes for the most upstream activator of the G 1 /S transition. Osmotic shock to cells synchronized in early G 1 , when Cln3 is the only cyclin present, causes a delay in cell cycle resumption. This points to Cln3 as being a key cell cycle target for osmotic stress. We have observed that osmotic shock causes downregulation of the kinase activity of Cln3–Cdc28 complexes. This is concomitant with a temporary accumulation of Cln3 protein as a result of increased stability. The effects of the osmotic stress in G 1 are not suppressed in CLN3‐1 cells with increased kinase activity, as the Cln3–Cdc28 activity in this mutant is still affected by the shock. Although Hog1 is not required for the observed cell cycle arrest in hyperosmotic conditions, it is necessary to resume the cell cycle at KCl concentrations higher than 0.4 M.