Mutations in SNF1 complex genes affect yeast cell wall strength

Autor(en): Backhaus, Katja
Rippert, Dorthe 
Heilmann, Clemens J.
Sorgo, Alice G.
de Koster, Chris G.
Klis, Frans M.
Rodicio, Rosaura
Heinisch, Juergen J.
Stichwörter: ACTIVATION; Cell Biology; Cell wall thickness; CWI signaling; GENOME-WIDE; Glucose signaling; INTEGRITY; INVASIVE GROWTH; Metabolism; PATHWAYS; PHOSPHOFRUCTOKINASE; PHOSPHORYLATION; PROTEIN-KINASE-C; SACCHAROMYCES-CEREVISIAE; STRESS
Erscheinungsdatum: 2013
Herausgeber: ELSEVIER GMBH
Journal: EUROPEAN JOURNAL OF CELL BIOLOGY
Volumen: 92
Ausgabe: 12
Startseite: 383
Seitenende: 395
Zusammenfassung: 
The trimeric SNF1 complex from Saccharomyces cerevisiae, a homolog of mammalian AMP-activated kinase, has been primarily implicated in signaling for the utilization of alternative carbon sources to glucose. We here find that snf1 deletion mutants are hypersensitive to different cell wall stresses, such as the presence of Calcofluor white, Congo red, Zymolyase or the glucan synthase inhibitor Caspofungin in the growth medium. They also have a thinner cell wall. Caspofungin treatment triggers the phosphorylation of the catalytic Snf1 kinase subunit at Thr210 and removal of this phosphorylation site by mutagenesis (Snf1-T210A) abolishes the function of Snf1 in cell wall integrity. Deletion of the PFK1 gene encoding the alpha-subunit of the heterooctameric yeast phosphofructokinase suppresses the cell wall phenotypes of a snf1 deletion, which suggests a compensatory effect of central carbohydrate metabolism. Epistasis analyses with mutants in cell wall integrity (CWI) signaling confirm that the SNF1 complex and the CWI pathway independently affect yeast cell integrity. (c) 2014 Elsevier GmbH. All rights reserved.
ISSN: 01719335
DOI: 10.1016/j.ejcb.2014.01.001

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