Characterization of glycogen-deficient glc mutants of Saccharomyces cerevisiae.

Abstract

Forty-eight mutants of Saccharomyces cerevisiae with defects in glycogen metabolism were isolated. The mutations defined eight GLC genes, the function of which were determined. Mutations in three of these genes activate the RAS/cAMP pathway either by impairment of a RAS GTPase-activating protein (GLC1/IRA1 and GLC4/IRA2) or by activating Ras2p (GLC5/RAS2). SNF1 protein kinase (GLC2) was found to be required for normal glycogen levels. Glycogen branching enzyme (GLC3) was found to be required for significant glycogen synthesis. GLC6 was shown to be allelic to CIF1 (and probably FDP1, BYP1 and GGS1), mutations in which were previously found to prevent growth on glucose; this gene is also the same as TPS1, which encodes a subunit of the trehalose-phosphate synthase. Mutations in GLC6 were capable of increasing or decreasing glycogen levels, at least in part via effects on the regulation of glycogen synthase. GLC7 encodes a type 1 protein phosphatase that contributes to the dephosphorylation (and hence activation) of glycogen synthase. GLC8 encodes a homologue of type 1 protein phosphatase inhibitor-2. The genetic map positions of GLC1/IRA1, GLC3, GLC4/IRA2, GLC6/CIF1/TPS1 (and the adjacent VAT2/VMA2), and GLC7 were clarified. From the data on GLC3, there may be a suppression of recombination near the chromosome V centromere, at least in some strains.

A CRISPR Interference Screen of Essential Genes Reveals that Proteasome Regulation Dictates Acetic Acid Tolerance in Saccharomyces cerevisiae

“…The accumulation of the storage carbohydrate glycogen has previously been reported to be critical for growth under acetic acid stress ( 23 , 24 ). GLC7 encodes a type 1 protein phosphatase that contributes to the dephosphorylation and, hence, the activation of glycogen synthases ( 25 ). We found that 3 out of 5 strains with gRNAs targeting GLC7 showed significant acetic acid sensitivity, increasing the relative generation time by 16 to 120% ( Fig.…”

“…Glycogen serves as a fuel reserve for cells and accumulates when growth conditions deteriorate as a means of adapting to stress such as nutrient, carbon, or energy limitation ( 47 ) or acetic acid treatment ( 23 , 24 ). Glycogen is produced from glucose-6-phosphate via glycogen synthases that are activated by dephosphorylation by, e.g., the Glc7 phosphatase ( 25 ).…”

AMPK β Subunit Targets Metabolic Stress Sensing to Glycogen

“…To study the subcellular localization AMPK to glycogen metabolism. The yeast homolog Snf1p is important for maintaining glycogen levels [22]. of the AMPK ␤1 subunit, we transiently expressed ␤1-GFP in COS-7 cells together with glycogen phosphory-Glycogen synthase, an AMPK substrate [19], and glycogen phosphorylase coimmunoprecipitate with AMPK lase (GP) tagged to Discosoma sp.…”

A CRISPRi screen of essential genes reveals that proteasome regulation dictates acetic acid tolerance inSaccharomyces cerevisiae

“…Accumulation of the storage carbohydrate glycogen has earlier been reported to be critical for growth under acetic acid stress (23,24). GLC7 encodes a type 1 protein phosphatase that contributes to the dephosphorylation and hence activation of glycogen synthases (25). We found that 3 out of 5 strains with gRNAs targeting GLC7 showed significant acetic acid sensitivity, increasing the relative generation time by 16-120% (Fig.…”