ArticleMolecular and cellular biology2004
Mutations in the gal83 glycogen-binding domain activate the snf1/gal83 kinase pathway by a glycogen-independent mechanism.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 50 citations in OpenAlex.
- A genetic screen reveals a key role for Reg1 in 2-deoxyglucose sensing and yeast AMPK inhibition.PLoS genetics · 2025Article
- Bacterial amylases enable glycogen degradation by the vaginal microbiome.Nature microbiology · 2023Article
- Comparative proteomics reveals the mechanism of cyclosporine production and mycelial growth inFrontiers in microbiology · 2023Article
- The Regulatory Role of Key Metabolites in the Control of Cell Signaling.Biomolecules · 2020Review
- Laboratory evolution for forced glucose-xylose co-consumption enables identification of mutations that improve mixed-sugar fermentation by xylose-fermenting Saccharomyces cerevisiae.FEMS yeast research · 2018Article
- The recruitment of AMP-activated protein kinase to glycogen is regulated by autophosphorylation.The Journal of biological chemistry · 2015Article
- Mechanisms of regulation of SNF1/AMPK/SnRK1 protein kinases.Frontiers in plant science · 2014Review
- The hybrid four-CBS-domain KINβγ subunit functions as the canonical γ subunit of the plant energy sensor SnRK1.The Plant journal : for cell and molecular biology · 2013Article
- Purification, characterization and cloning of a thermotolerant isoamylase produced from Bacillus sp. CICIM 304.Journal of industrial microbiology & biotechnology · 2013Article
- Heterotrimer-independent regulation of activation-loop phosphorylation of Snf1 protein kinase involves two protein phosphatases.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Alterations at dispersed sites cause phosphorylation and activation of SNF1 protein kinase during growth on high glucose.The Journal of biological chemistry · 2011Article
- Roles of two protein phosphatases, Reg1-Glc7 and Sit4, and glycogen synthesis in regulation of SNF1 protein kinase.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Regulation of glycogen metabolism in yeast and bacteria.FEMS microbiology reviews · 2010Review
- Roles of the glycogen-binding domain and Snf4 in glucose inhibition of SNF1 protein kinase.The Journal of biological chemistry · 2008Article
- SNF1/AMPK pathways in yeast.Frontiers in bioscience : a journal and virtual library · 2008Review
- Regulation of the nucleocytoplasmic distribution of Snf1-Gal83 protein kinase.Eukaryotic cell · 2006Article
- AKINbetagamma contributes to SnRK1 heterotrimeric complexes and interacts with two proteins implicated in plant pathogen resistance through its KIS/GBD sequence.Plant physiology · 2006Article
- Gene expression profiling of mice with genetically modified muscle glycogen content.The Biochemical journal · 2006Article
- Role of Tos3, a Snf1 protein kinase kinase, during growth of Saccharomyces cerevisiae on nonfermentable carbon sources.Eukaryotic cell · 2005Article
- AKINbeta3, a plant specific SnRK1 protein, is lacking domains present in yeast and mammals non-catalytic beta-subunits.Plant molecular biology · 2004Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The yeast Snf1 kinase and its mammalian ortholog, AMP-activated protein kinase (AMPK), regulate responses to metabolic stress. Previous studies identified a glycogen-binding domain in the AMPK beta1 subunit, and the sequence is conserved in the Snf1 kinase beta subunits Gal83 and Sip2. Here we use genetic analysis to assess the role of this domain in vivo. Alteration of Gal83 at residues that are important for glycogen binding of AMPK beta1 abolished glycogen binding in vitro and caused diverse phenotypes in vivo. Various Snf1/Gal83-dependent processes were upregulated, including glycogen accumulation, expression of RNAs encoding glycogen synthase, haploid invasive growth, the transcriptional activator function of Sip4, and activation of the carbon source-responsive promoter element. Moreover, the glycogen-binding domain mutations conferred transcriptional regulatory phenotypes even in the absence of glycogen, as determined by analysis of a mutant strain lacking glycogen synthase. Thus, mutation of the glycogen-binding domain of Gal83 positively affects Snf1/Gal83 kinase function by a mechanism that is independent of glycogen binding.
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