ArticleMolecular biology of the cell2016
The glucose metabolite methylglyoxal inhibits expression of the glucose transporter genes by inactivating the cell surface glucose sensors Rgt2 and Snf3 in yeast.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- The advances in creating Crabtree-negative Saccharomyces cerevisiae and the application for chemicals biosynthesis.FEMS yeast research · 2025Review
- Clinical, Neuroimaging, and Metabolic Footprint of the Neurodevelopmental Disorder Caused by MonoallelicNeurology. Genetics · 2024Article
- Multiple roles for the cytoplasmic C-terminal domains of the yeast cell surface receptors Rgt2 and Snf3 in glucose sensing and signaling.Scientific reports · 2024Article
- Controlling circuitry underlies the growth optimization of Saccharomyces cerevisiae.Metabolic engineering · 2023Article
- Transcriptional Response of Candida auris to the Mrr1 Inducers Methylglyoxal and Benomyl.mSphere · 2022Article
- Casein kinases are required for the stability of the glucose-sensing receptor Rgt2 in yeast.Scientific reports · 2022Article
- mTOR-dependent dysregulation of autophagy contributes to the retinal ganglion cell loss in streptozotocin-induced diabetic retinopathy.Cell communication and signaling : CCS · 2021Article
- Ethanol tolerance assessment in recombinant E. coli of ethanol responsive genes from Lactobacillus buchneri NRRL B-30929.World journal of microbiology & biotechnology · 2020Article
- Reactive Carbonyls Induce TOR- and Carbohydrate-Dependent Hormetic Response in Yeast.TheScientificWorldJournal · 2020Article
- Phenylpyrrole fungicides act on triosephosphate isomerase to induce methylglyoxal stress and alter hybrid histidine kinase activity.Scientific reports · 2019Article
- Trees, fungi and bacteria: tripartite metatranscriptomics of a root microbiome responding to soil contamination.Microbiome · 2018Article
- Ask yeast how to burn your fats: lessons learned from the metabolic adaptation to salt stress.Current genetics · 2018Review
- The apple polyphenol phloretin inhibits breast cancer cell migration and proliferation via inhibition of signals by type 2 glucose transporter.Journal of food and drug analysis · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Methylglyoxal (MG) is a cytotoxic by-product of glycolysis. MG has inhibitory effect on the growth of cells ranging from microorganisms to higher eukaryotes, but its molecular targets are largely unknown. The yeast cell-surface glucose sensors Rgt2 and Snf3 function as glucose receptors that sense extracellular glucose and generate a signal for induction of expression of genes encoding glucose transporters (HXTs). Here we provide evidence that these glucose sensors are primary targets of MG in yeast. MG inhibits the growth of glucose-fermenting yeast cells by inducing endocytosis and degradation of the glucose sensors. However, the glucose sensors with mutations at their putative ubiquitin-acceptor lysine residues are resistant to MG-induced degradation. These results suggest that the glucose sensors are inactivated through ubiquitin-mediated endocytosis and degraded in the presence of MG. In addition, the inhibitory effect of MG on the glucose sensors is greatly enhanced in cells lacking Glo1, a key component of the MG detoxification system. Thus the stability of these glucose sensors seems to be critically regulated by intracellular MG levels. Taken together, these findings suggest that MG attenuates glycolysis by promoting degradation of the cell-surface glucose sensors and thus identify MG as a potential glycolytic inhibitor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.