Premium
Multiple signalling pathways trigger the exquisite sensitivity of yeast gluconeogenic mRNAs to glucose
Author(s) -
Yin Zhikang,
Smith Rachel J.,
Brown Alistair J. P.
Publication year - 1996
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 - 10.1111/j.1365-2958.1996.tb02514.x
Subject(s) - biology , snf3 , psychological repression , phosphoenolpyruvate carboxykinase , fructose 1,6 bisphosphatase , mutant , catabolite repression , glucokinase , biochemistry , gluconeogenesis , hexokinase , saccharomyces cerevisiae , microbiology and biotechnology , yeast , fructose , glycolysis , gene , gene expression , enzyme
Summary The transcription of the yeast FBP1 and PCK1 genes, which encode the gluconeogenic enzymes fructose‐1,6‐bisphosphatase and phosphoenolpyruvate car‐boxykinase, is repressed by glucose. Here, we show that this repression is both very strong and exceptionally sensitive to glucose, being triggered by glucose at concentrations less than 0.005% (0.27 mM). This repression remains operative in yeast mutants carrying any one of the three hexose kinases, but is lost in a triple hxk1, hxk2, glk1 mutant. In addition, 2‐deoxyglucose can trigger the repression, but 6‐deoxy‐glucose cannot, suggesting that internalization and phosphorylation of the glucose is essential for repression to occur. While gluconeogenic gene transcription is subject to the Mig1p‐dependent pathway of glucose repression, the exquisite response to glucose is maintained in hxk2 and mig1 mutants, suggesting that this pathway is not essential for the response. The response can also be triggered by the addition of exogenous cAMP, suggesting that the Ras/cAMP pathway can mediate repression of the FPB1 and PCK1 mRNAs. However, the response is not dependent upon this pathway because it remains intact in Ras, adenyl cyclase and protein kinase A mutants. The data show that yeast cells can detect very low glucose concentrations in the environment, and suggest that several distinct signalling pathways operate to repress FPB1 and PCK1 transcription in the presence of glucose.