Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.

Glucose is central to many biological processes, serving as an energy source and a building block for biosynthesis. After glucose enters the cell, hexokinases convert it to glucose-6-phosphate (Glc-6P) for use in anaerobic fermentation, aerobic oxidative phosphorylation, and the pentose-phosphate pa...

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Main Authors: Erich Hellemann, Jennifer L Walker, Mitchell A Lesko, Dakshayini G Chandrashekarappa, Martin C Schmidt, Allyson F O'Donnell, Jacob D Durrant
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2022-03-01
Series:PLoS Computational Biology
Online Access:https://journals.plos.org/ploscompbiol/article/file?id=10.1371/journal.pcbi.1009929&type=printable
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author Erich Hellemann
Jennifer L Walker
Mitchell A Lesko
Dakshayini G Chandrashekarappa
Martin C Schmidt
Allyson F O'Donnell
Jacob D Durrant
author_facet Erich Hellemann
Jennifer L Walker
Mitchell A Lesko
Dakshayini G Chandrashekarappa
Martin C Schmidt
Allyson F O'Donnell
Jacob D Durrant
author_sort Erich Hellemann
collection DOAJ
description Glucose is central to many biological processes, serving as an energy source and a building block for biosynthesis. After glucose enters the cell, hexokinases convert it to glucose-6-phosphate (Glc-6P) for use in anaerobic fermentation, aerobic oxidative phosphorylation, and the pentose-phosphate pathway. We here describe a genetic screen in Saccharomyces cerevisiae that generated a novel spontaneous mutation in hexokinase-2, hxk2G238V, that confers resistance to the toxic glucose analog 2-deoxyglucose (2DG). Wild-type hexokinases convert 2DG to 2-deoxyglucose-6-phosphate (2DG-6P), but 2DG-6P cannot support downstream glycolysis, resulting in a cellular starvation-like response. Curiously, though the hxk2G238V mutation encodes a loss-of-function allele, the affected amino acid does not interact directly with bound glucose, 2DG, or ATP. Molecular dynamics simulations suggest that Hxk2G238V impedes sugar binding by altering the protein dynamics of the glucose-binding cleft, as well as the large-scale domain-closure motions required for catalysis. These findings shed new light on Hxk2 dynamics and highlight how allosteric changes can influence catalysis, providing new structural insights into this critical regulator of carbohydrate metabolism. Given that hexokinases are upregulated in some cancers and that 2DG and its derivatives have been studied in anti-cancer trials, the present work also provides insights that may apply to cancer biology and drug resistance.
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publisher Public Library of Science (PLoS)
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spelling doaj-art-15f4c4e3c2344d9089e14c5d30a5d4e82025-08-20T03:15:48ZengPublic Library of Science (PLoS)PLoS Computational Biology1553-734X1553-73582022-03-01183e100992910.1371/journal.pcbi.1009929Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.Erich HellemannJennifer L WalkerMitchell A LeskoDakshayini G ChandrashekarappaMartin C SchmidtAllyson F O'DonnellJacob D DurrantGlucose is central to many biological processes, serving as an energy source and a building block for biosynthesis. After glucose enters the cell, hexokinases convert it to glucose-6-phosphate (Glc-6P) for use in anaerobic fermentation, aerobic oxidative phosphorylation, and the pentose-phosphate pathway. We here describe a genetic screen in Saccharomyces cerevisiae that generated a novel spontaneous mutation in hexokinase-2, hxk2G238V, that confers resistance to the toxic glucose analog 2-deoxyglucose (2DG). Wild-type hexokinases convert 2DG to 2-deoxyglucose-6-phosphate (2DG-6P), but 2DG-6P cannot support downstream glycolysis, resulting in a cellular starvation-like response. Curiously, though the hxk2G238V mutation encodes a loss-of-function allele, the affected amino acid does not interact directly with bound glucose, 2DG, or ATP. Molecular dynamics simulations suggest that Hxk2G238V impedes sugar binding by altering the protein dynamics of the glucose-binding cleft, as well as the large-scale domain-closure motions required for catalysis. These findings shed new light on Hxk2 dynamics and highlight how allosteric changes can influence catalysis, providing new structural insights into this critical regulator of carbohydrate metabolism. Given that hexokinases are upregulated in some cancers and that 2DG and its derivatives have been studied in anti-cancer trials, the present work also provides insights that may apply to cancer biology and drug resistance.https://journals.plos.org/ploscompbiol/article/file?id=10.1371/journal.pcbi.1009929&type=printable
spellingShingle Erich Hellemann
Jennifer L Walker
Mitchell A Lesko
Dakshayini G Chandrashekarappa
Martin C Schmidt
Allyson F O'Donnell
Jacob D Durrant
Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.
PLoS Computational Biology
title Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.
title_full Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.
title_fullStr Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.
title_full_unstemmed Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.
title_short Novel mutation in hexokinase 2 confers resistance to 2-deoxyglucose by altering protein dynamics.
title_sort novel mutation in hexokinase 2 confers resistance to 2 deoxyglucose by altering protein dynamics
url https://journals.plos.org/ploscompbiol/article/file?id=10.1371/journal.pcbi.1009929&type=printable
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