Year: 2017
Type: article
Abstract: Glycolysis is upregulated under conditions such as hypoxia and high energy demand to promote cell proliferation, although the mechanism remains poorly understood. We find that hypoxia in Saccharomyces cerevisiae induces concentration of glycolytic enzymes, including the Pfk2p subunit of the rate-limiting phosphofructokinase, into a single, non-membrane-bound granule termed the "glycolytic body" or "G body." A yeast kinome screen identifies the yeast ortholog of AMP-activated protein kinase, Snf1p, as necessary for G-body formation. Many G-body components identified by proteomics are required for G-body integrity. Cells incapable of forming G bodies in hypoxia display abnormal cell division and produce inviable daughter cells. Conversely, cells with G bodies show increased glucose consumption and decreased levels of glycolytic intermediates. Importantly, G bodies form in human hepatocarcinoma cells in hypoxia. Together, our results suggest that G body formation is a conserved, adaptive response to increase glycolytic output during hypoxia or tumorigenesis.
Source: Cell Reports
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $5,620
Awards: G1492615674, Michigan Regional Comprehensive Metabolomics Resource Core (MRC2), Michigan Predoctoral Training in Genetics, Comprehensive Biology: Exploiting the Yeast Genome, Role of mTORC1 pathway for podocyte injury in diabetic nephropathy, Comprehensive Biology: Exploiting the Yeast Genome, G4449404171, The role of post-translational modifications in miRISC function, Regulation of Gene Expression by microRNAs in C. elegans, Molecular mechanism of mTORC1-dependent translation and ribosome biogenesis, Cellular and Molecular Biology, Alternative Vacuolar Targeting Mechanisms in Yeast, Lysosomal cholesterol-dependent anabolic regulation
OpenAlex ID: W2738634672