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Transcriptional responses to glucose at different glycolytic rates in Saccharomyces cerevisiae

Journal article
Authors Karin Elbing
Anders Ståhlberg
Stefan Hohmann
Lena Gustafsson
Published in European Journal of Biochemistry
Volume 271
Issue 23-24
Pages 4855-4864
ISSN 0014-2956
Publication year 2004
Published at Department of Cell and Molecular Biology
Pages 4855-4864
Language en
Links dx.doi.org/10.1111/j.1432-1033.2004...
Keywords saccharomyces cerevisiae, mig1, snf1, glucose repression, glucose signal, snf1 protein-kinase, catabolite repression, fermentative capacity, chemostat cultures, yeast hexokinase, upstream kinases, messenger-rnas, budding yeast, phosphorylation, activation
Subject categories Cell and molecular biology

Abstract

The addition of glucose to Saccharomyces cerevisiae cells causes reprogramming of gene expression. Glucose is sensed by membrane receptors as well as (so far elusive) intracellular sensing mechanisms. The availability of four yeast strains that display different hexose uptake capacities allowed us to study glucose-induced effects at different glycolytic rates. Rapid glucose responses were observed in all strains able to take up glucose, consistent with intracellular sensing. The degree of long-term responses, however, clearly correlated with the glycolytic rate: glucose-stimulated expression of genes encoding enzymes of the lower part of glycolysis showed an almost linear correlation with the glycolytic rate, while expression levels of genes encoding gluconeogenic enzymes and invertase (SUC2) showed an inverse correlation. Glucose control of SUC2 expression is mediated by the Snf1-Mig1 pathway. Mig1 dephosphorylation upon glucose addition is known to lead to repression of target genes. Mig1 was initially dephosphorylated upon glucose addition in all strains able to take up glucose, but remained dephosphorylated only at high glycolytic rates. Remarkably, transient Mig1-dephosphorylation was accompanied by the repression of SUC2 expression at high glycolytic rates, but stimulated SUC2 expression at low glycolytic rates. This suggests that Mig1-mediated repression can be overruled by factors mediating induction via a low glucose signal. At low and moderate glycolytic rates, Mig1 was partly dephosphorylated both in the presence of phosphorylated, active Snf1, and unphosphorylated, inactive Snf1, indicating that Mig1 was actively phosphorylated and dephosphorylated simultaneously, suggesting independent control of both processes. Taken together, it appears that glucose addition affects the expression of SUC2 as well as Mig1 activity by both Snf1-dependent and -independent mechanisms that can now be dissected and resolved as early and late/sustained responses.

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