Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism
- Publikationstyp:
- Zeitschriftenaufsatz
- Metadaten:
-
- Autoren
- Matteo Fumagalli
- Stephane M Camus
- Yoan Diekmann
- Alice Burke
- Marine D Camus
- Paul J Norman
- Agnel Joseph
- Laurent Abi-Rached
- Andrea Benazzo
- Rita Rasteiro
- Iain Mathieson
- Maya Topf
- Peter Parham
- Mark G Thomas
- Frances M Brodsky
- Autoren-URL
- https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000470717600001&DestLinkType=FullRecord&DestApp=WOS_CPL
- DOI
- 10.7554/eLife.41517
- Externe Identifier
- Clarivate Analytics Document Solution ID: IC1KH
- PubMed Identifier: 31159924
- ISSN
- 2050-084X
- Zeitschrift
- ELIFE
- Artikelnummer
- ARTN e41517
- Datum der Veröffentlichung
- 2019
- Status
- Published
- Titel
- Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism
- Sub types
- Article
- Ausgabe der Zeitschrift
- 8
Datenquelle: Web of Science (Lite)
- Andere Metadatenquellen:
-
- Abstract
- <jats:p>CHC22 clathrin plays a key role in intracellular membrane traffic of the insulin-responsive glucose transporter GLUT4 in humans. We performed population genetic and phylogenetic analyses of the CHC22-encoding CLTCL1 gene, revealing independent gene loss in at least two vertebrate lineages, after arising from gene duplication. All vertebrates retained the paralogous CLTC gene encoding CHC17 clathrin, which mediates endocytosis. For vertebrates retaining CLTCL1, strong evidence for purifying selection supports CHC22 functionality. All human populations maintained two high frequency CLTCL1 allelic variants, encoding either methionine or valine at position 1316. Functional studies indicated that CHC22-V1316, which is more frequent in farming populations than in hunter-gatherers, has different cellular dynamics than M1316-CHC22 and is less effective at controlling GLUT4 membrane traffic, altering its insulin-regulated response. These analyses suggest that ancestral human dietary change influenced selection of allotypes that affect CHC22’s role in metabolism and have potential to differentially influence the human insulin response.</jats:p>
- Autoren
- Matteo Fumagalli
- Stephane M Camus
- Yoan Diekmann
- Alice Burke
- Marine D Camus
- Paul J Norman
- Agnel Joseph
- Laurent Abi-Rached
- Andrea Benazzo
- Rita Rasteiro
- Iain Mathieson
- Maya Topf
- Peter Parham
- Mark G Thomas
- Frances M Brodsky
- DOI
- 10.7554/elife.41517
- eISSN
- 2050-084X
- Zeitschrift
- eLife
- Sprache
- en
- Online publication date
- 2019
- Status
- Published online
- Herausgeber
- eLife Sciences Publications, Ltd
- Herausgeber URL
- http://dx.doi.org/10.7554/elife.41517
- Datum der Datenerfassung
- 2023
- Titel
- Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism
- Ausgabe der Zeitschrift
- 8
Datenquelle: Crossref
- Abstract
- CHC22 clathrin plays a key role in intracellular membrane traffic of the insulin-responsive glucose transporter GLUT4 in humans. We performed population genetic and phylogenetic analyses of the CHC22-encoding <i>CLTCL1</i> gene, revealing independent gene loss in at least two vertebrate lineages, after arising from gene duplication. All vertebrates retained the paralogous <i>CLTC</i> gene encoding CHC17 clathrin, which mediates endocytosis. For vertebrates retaining <i>CLTCL1</i>, strong evidence for purifying selection supports CHC22 functionality. All human populations maintained two high frequency <i>CLTCL1</i> allelic variants, encoding either methionine or valine at position 1316. Functional studies indicated that CHC22-V1316, which is more frequent in farming populations than in hunter-gatherers, has different cellular dynamics than M1316-CHC22 and is less effective at controlling GLUT4 membrane traffic, altering its insulin-regulated response. These analyses suggest that ancestral human dietary change influenced selection of allotypes that affect CHC22's role in metabolism and have potential to differentially influence the human insulin response.
- Addresses
- Department of Life Sciences, Imperial College London, Ascot, United Kingdom.
- Autoren
- Matteo Fumagalli
- Stephane M Camus
- Yoan Diekmann
- Alice Burke
- Marine D Camus
- Paul J Norman
- Agnel Joseph
- Laurent Abi-Rached
- Andrea Benazzo
- Rita Rasteiro
- Iain Mathieson
- Maya Topf
- Peter Parham
- Mark G Thomas
- Frances M Brodsky
- DOI
- 10.7554/elife.41517
- eISSN
- 2050-084X
- Externe Identifier
- PubMed Identifier: 31159924
- PubMed Central ID: PMC6548504
- Funding acknowledgements
- Wellcome Trust: 107858/Z/15/Z
- NIH HHS: AI090905
- National Institutes of Health: DK095663
- NIDDK NIH HHS: R01 DK095663
- Medical Research Council: MR/S008144/1
- Wellcome Trust:
- NIAID NIH HHS: U01 AI090905
- NIH HHS: DK095663
- National Institutes of Health: AI090905
- Open access
- true
- ISSN
- 2050-084X
- Zeitschrift
- eLife
- Schlüsselwörter
- Humans
- Glucose
- Clathrin Heavy Chains
- Diet
- Evolution, Molecular
- Alleles
- Genetic Variation
- Selection, Genetic
- Sprache
- eng
- Medium
- Electronic
- Online publication date
- 2019
- Open access status
- Open Access
- Paginierung
- e41517
- Datum der Veröffentlichung
- 2019
- Status
- Published
- Publisher licence
- CC BY
- Datum der Datenerfassung
- 2019
- Titel
- Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism.
- Sub types
- Research Support, Non-U.S. Gov't
- research-article
- Journal Article
- Research Support, N.I.H., Extramural
- Ausgabe der Zeitschrift
- 8
Files
https://europepmc.org/articles/PMC6548504?pdf=render
Datenquelle: Europe PubMed Central
- Abstract
- CHC22 clathrin plays a key role in intracellular membrane traffic of the insulin-responsive glucose transporter GLUT4 in humans. We performed population genetic and phylogenetic analyses of the CHC22-encoding CLTCL1 gene, revealing independent gene loss in at least two vertebrate lineages, after arising from gene duplication. All vertebrates retained the paralogous CLTC gene encoding CHC17 clathrin, which mediates endocytosis. For vertebrates retaining CLTCL1, strong evidence for purifying selection supports CHC22 functionality. All human populations maintained two high frequency CLTCL1 allelic variants, encoding either methionine or valine at position 1316. Functional studies indicated that CHC22-V1316, which is more frequent in farming populations than in hunter-gatherers, has different cellular dynamics than M1316-CHC22 and is less effective at controlling GLUT4 membrane traffic, altering its insulin-regulated response. These analyses suggest that ancestral human dietary change influenced selection of allotypes that affect CHC22's role in metabolism and have potential to differentially influence the human insulin response.
- Date of acceptance
- 2019
- Autoren
- Matteo Fumagalli
- Stephane M Camus
- Yoan Diekmann
- Alice Burke
- Marine D Camus
- Paul J Norman
- Agnel Joseph
- Laurent Abi-Rached
- Andrea Benazzo
- Rita Rasteiro
- Iain Mathieson
- Maya Topf
- Peter Parham
- Mark G Thomas
- Frances M Brodsky
- Autoren-URL
- https://www.ncbi.nlm.nih.gov/pubmed/31159924
- DOI
- 10.7554/eLife.41517
- eISSN
- 2050-084X
- Externe Identifier
- PubMed Central ID: PMC6548504
- Funding acknowledgements
- Medical Research Council: MR/S008144/1
- Wellcome Trust: 107858/Z/15/Z
- NIDDK NIH HHS: R01 DK095663
- NIAID NIH HHS: U01 AI090905
- NIH HHS: DK095663
- NIH HHS: AI090905
- Wellcome Trust:
- Zeitschrift
- Elife
- Schlüsselwörter
- cell biology
- evolutionary biology
- evolutionary selection
- human
- insulin response
- membrane traffic
- Alleles
- Clathrin Heavy Chains
- Diet
- Evolution, Molecular
- Genetic Variation
- Glucose
- Humans
- Selection, Genetic
- Sprache
- eng
- Country
- England
- PII
- 41517
- Datum der Veröffentlichung
- 2019
- Status
- Published online
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2020
- Titel
- Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism.
- Sub types
- Journal Article
- Research Support, N.I.H., Extramural
- Research Support, Non-U.S. Gov't
- Ausgabe der Zeitschrift
- 8
Datenquelle: PubMed
- Beziehungen:
- Eigentum von