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Sökning: id:"swepub:oai:gup.ub.gu.se/40216" > Transcriptional res...

Transcriptional responses to glucose at different glycolytic rates in Saccharomyces cerevisiae

Elbing, Karin, 1974 (författare)
Chalmers tekniska högskola,Chalmers University of Technology
Ståhlberg, Anders, 1975 (författare)
Chalmers tekniska högskola,Chalmers University of Technology
Hohmann, Stefan, 1956 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för cell- och molekylärbiologi,Department of Cell and Molecular Biology,University of Gothenburg
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Gustafsson, Lena, 1949 (författare)
Chalmers tekniska högskola,Chalmers University of Technology
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 (creator_code:org_t)
Wiley, 2004
2004
Engelska.
Ingår i: European Journal of Biochemistry. - : Wiley. - 0014-2956 .- 1432-1033. ; 271:23-24, s. 4855-4864
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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.

Ämnesord

NATURVETENSKAP  -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
NATURAL SCIENCES  -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)

Nyckelord

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
chemostat cultures

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