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Coordinated regulation of intracellular pH by two glucose-sensing pathways in yeast.

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Title: Coordinated regulation of intracellular pH by two glucose-sensing pathways in yeast.
Authors: Isom, Daniel G.1,2 disom@miami.edu, Page, Stephani C.1, Collins, Leonard B.3, Kapolka, Nicholas J.2, Taghon, Geoffrey J.2, Dohlman, Henrik G.1 hdohlman@med.unc.edu
Source: Journal of Biological Chemistry. 2/16/2018, Vol. 293 Issue 7, p2318-2329. 12p.
Subjects: Glucose-regulated proteins, Saccharomyces cerevisiae, Cellular control mechanisms, Cellular signal transduction, Proton pump inhibitors, Cytoplasmic filaments, Fungi
Abstract: The yeast Saccharomyces cerevisiae employs multiple pathways to coordinate sugar availability and metabolism. Glucose and other sugars are detected by a G protein-coupled receptor, Gpr1, as well as a pair of transporter-like proteins, Rgt2 and Snf3. When glucose is limiting, however, an ATP-driven proton pump (Pma1) is inactivated, leading to a marked decrease in cytoplasmic pH. Here we determine the relative contribution of the two sugar-sensing pathways to pH regulation. Whereas cytoplasmic pH is strongly dependent on glucose abundance and is regulated by both glucose-sensing pathways, ATP is largely unaffected and therefore cannot account for the changes in Pma1 activity. These data suggest that the pH is a second messenger of the glucose-sensing pathways. We show further that different sugars differ in their ability to control cellular acidification, in the manner of inverse agonists. We conclude that the sugar-sensing pathways act via Pma1 to invoke coordinated changes in cellularpHand metabolism. Morebroadly, our findings support the emerging view that cellular systems have evolved the use of pH signals as a means of adapting to environmental stresses such as those caused by hypoxia, ischemia, and diabetes. [ABSTRACT FROM AUTHOR]
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Database: Engineering Source
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Abstract:The yeast Saccharomyces cerevisiae employs multiple pathways to coordinate sugar availability and metabolism. Glucose and other sugars are detected by a G protein-coupled receptor, Gpr1, as well as a pair of transporter-like proteins, Rgt2 and Snf3. When glucose is limiting, however, an ATP-driven proton pump (Pma1) is inactivated, leading to a marked decrease in cytoplasmic pH. Here we determine the relative contribution of the two sugar-sensing pathways to pH regulation. Whereas cytoplasmic pH is strongly dependent on glucose abundance and is regulated by both glucose-sensing pathways, ATP is largely unaffected and therefore cannot account for the changes in Pma1 activity. These data suggest that the pH is a second messenger of the glucose-sensing pathways. We show further that different sugars differ in their ability to control cellular acidification, in the manner of inverse agonists. We conclude that the sugar-sensing pathways act via Pma1 to invoke coordinated changes in cellularpHand metabolism. Morebroadly, our findings support the emerging view that cellular systems have evolved the use of pH signals as a means of adapting to environmental stresses such as those caused by hypoxia, ischemia, and diabetes. [ABSTRACT FROM AUTHOR]
ISSN:00219258
DOI:10.1074/jbc.RA117.000422