ITEM METADATA RECORD
Title: cAMP-PKA and Snf1 signaling mechanisms underlie the superior potency of sucrose for induction of filamentation in yeast
Authors: Van de Velde, Sam ×
Thevelein, Johan #
Issue Date: 21-Aug-2007
Publisher: American Society for Microbiology (ASM)
Series Title: Eukaryotic cell vol:7 issue:2 pages:286-293
Abstract: Under specific environmental conditions, the yeast Saccharomyces cerevisiae can undergo a morphological switch to a pseudohyphal growth pattern. Pseudohyphal differentiation is generally studied upon induction by nitrogen limitation in the presence of glucose. It is known to be controlled by several signaling pathways, including MAP kinase, cAMP-PKA and Snf1 kinase pathways. We show that the alpha-glucoside sugars maltose and maltotriose and especially sucrose are more potent inducers of filamentation than glucose. Sucrose even induces filamentation in nitrogen-rich media and in the mep2Delta/mep2Delta ammonium permease mutant on ammonium-limiting medium. We demonstrate that glucose also inhibits filamentation by means of a pathway parallel to the cAMP-PKA pathway. Deletion of HXK2 shifted the pseudohyphal growth pattern on glucose to that of sucrose, while deletion of SNF4 abrogated filamentation on both sugars, indicating a negative role of glucose repression and a positive role for Snf1 activity in the control of filamentation. In all strains and in all media, sucrose induction of filamentation is greatly diminished by deletion of the sucrose/glucose sensing GPCR Gpr1 whereas this has no effect on induction by maltose and maltotriose. The competence of alpha-glucoside sugars to induce filamentation is reflected in the increased expression of the cell surface flocculin FLO11. In addition, sucrose is the only alpha-glucoside sugar capable of rapidly inducing FLO11 expression in a Gpr1-dependent manner, reflecting the sensitivity of Gpr1 for this sugar and its involvement in rapid sucrose signaling. Our study identifies sucrose as the most potent nutrient inducer of pseudohyphal growth and shows that glucose inactivation of Snf1 kinase signaling is responsible for the lower potency of glucose.
URI: 
ISSN: 1535-9778
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular Microbiology and Biotechnology Section - miscellaneous
Laboratory for Molecular Cell Biology (-)
× corresponding author
# (joint) last author

Files in This Item:

There are no files associated with this item.

Request a copy

 




All items in Lirias are protected by copyright, with all rights reserved.

© Web of science