Abstract
Besides being the favorite carbon and energy source for the budding yeast Sacchromyces cerevisiae, glucose can act as a signaling molecule to regulate multiple aspects of yeast physiology. Yeast cells have evolved several mechanisms for monitoring the level of glucose in their habitat and respond quickly to frequent changes in the sugar availability in the environment: the cAMP/PKA pathways (with its two branches comprising Ras and the Gpr1/Gpa2 module), the Rgt2/Snf3-Rgt1 pathway and the main repression pathway involving the kinase Snf1. The cAMP/PKA pathway plays the prominent role in responding to changes in glucose availability and initiating the signaling processes that promote cell growth and division. Snf1 (the yeast homologous to mammalian AMP-activated protein kinase) is primarily required for the adaptation of yeast cell to glucose limitation and for growth on alternative carbon source, but it is also involved in the cellular response to various environmental stresses. The Rgt2/Snf3-Rgt1 pathway regulates the expression of genes required for glucose uptake. Many interconnections exist between the diverse glucose sensing systems, which enables yeast cells to fine tune cell growth, cell cycle and their coordination in response to nutritional changes.
Highlights
The budding yeast Saccharomyces cerevisiae is the first eukaryote whose genome was completely sequenced [1] and its ease of manipulation and the wide array of molecular and post-genomic techniques available make it a preferred model organism for genetic, biochemical and, more recently, systems biology studies [2,3,4]
Energetically less efficient than respiration, fermentation can proceed at much faster rates, allowing budding yeast to aggressively utilize glucose at the expenses of its energetically efficient but slower competitors: the rapid depletion of the sugar and the accumulation of large amounts of ethanol produced during fermentation enable yeast cells to successfully compete for survival
Multiple evidences support the notion that PKA contributes to glucose induction of HXT gene expression by catalyzing phosphorylation of Rgt1: i) PKA phosphorylates Rgt1 in vitro; ii) glucose fails to induce HXT genes expression in yeast cells with reduced PKA activity, whereas the transcription of HXTs is constitutive in strains with an hyperactive cAMP/PKA pathway; iii) several serine residues in the N-terminus of Rgt1, which are likely to be phosphorylated by PKA, are essential both for the intramolecular reaction of the repressor and for its release from the HXT promoter in response to glucose [33]
Summary
The budding yeast Saccharomyces cerevisiae is the first eukaryote whose genome was completely sequenced [1] and its ease of manipulation and the wide array of molecular and post-genomic techniques available make it a preferred model organism for genetic, biochemical and, more recently, systems biology studies [2,3,4]. Yeast cells express only the glucose transporters most appropriate for the amount of sugar available at any moment in the environment This pattern is due to the combined action of different regulatory mechanisms, including transcriptional regulation of the major HXT genes in response to glucose [11,13,14,15] and inactivation of Hxt proteins under appropriate conditions [16,17,18,19]. The glucose repression circuit that operates through the Snf protein kinase and the Mig transcriptional repressor prevents the expression of the high/intermediate affinity hexose carriers (encoded by HXT2, HXT4, HXT6 and HXT7) when the sugar levels are high [15,22]. Glucose phosphorylating enzymes (in particular Hxk2) appear to influence the expression pattern of the HXT genes [7,13,38,39,40,41]
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