The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic

Publication type:
Journal article
Metadata:
Autoren
  • Rachel E Turn
  • Yihan Hu
  • Skylar I Dewees
  • Narra Devi
  • Michael P East
  • Katherine R Hardin
  • Tala Khatib
  • Joshua Linnert
  • Uwe Wolfrum
  • Michael J Lim
  • James E Casanova
  • Tamara Caspary
  • Richard A Kahn
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000750968600003&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1091/mbc.E21-09-0443
eISSN
1939-4586
Externe Identifier
  • Clarivate Analytics Document Solution ID: YS9CI
  • PubMed Identifier: 34818063
ISSN
1059-1524
Ausgabe der Veröffentlichung
2
Zeitschrift
MOLECULAR BIOLOGY OF THE CELL
Artikelnummer
ARTN ar13
Datum der Veröffentlichung
2022
Status
Published
Titel
The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic
Sub types
  • Article
Ausgabe der Zeitschrift
33

Data source: Web of Science (Lite)

Other metadata sources:
Abstract
<jats:p> ELMODs are a highly conserved family of three mammalian paralogues that display GTPase-activating protein activity toward a uniquely broad array of ADP-ribosylation factor family GTPases. Here, we identify novel functions for ELMOD1 and ELMOD3 in ciliogenesis and Golgi-ciliary traffic, acting in the same pathway as ARL3 and ARL16. </jats:p>
Autoren
  • Rachel E Turn
  • Yihan Hu
  • Skylar I Dewees
  • Narra Devi
  • Michael P East
  • Katherine R Hardin
  • Tala Khatib
  • Joshua Linnert
  • Uwe Wolfrum
  • Michael J Lim
  • James E Casanova
  • Tamara Caspary
  • Richard A Kahn
DOI
10.1091/mbc.e21-09-0443
Editoren
  • Anne Spang
eISSN
1939-4586
ISSN
1059-1524
Ausgabe der Veröffentlichung
2
Zeitschrift
Molecular Biology of the Cell
Sprache
en
Datum der Veröffentlichung
2022
Status
Published
Herausgeber
American Society for Cell Biology (ASCB)
Herausgeber URL
http://dx.doi.org/10.1091/mbc.e21-09-0443
Datum der Datenerfassung
2022
Titel
The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic
Ausgabe der Zeitschrift
33

Data source: Crossref

Abstract
ELMODs are a family of three mammalian paralogues that display GTPase-activating protein (GAP) activity toward a uniquely broad array of ADP-ribosylation factor (ARF) family GTPases that includes ARF-like (ARL) proteins. ELMODs are ubiquitously expressed in mammalian tissues, highly conserved across eukaryotes, and ancient in origin, being present in the last eukaryotic common ancestor. We described functions of ELMOD2 in immortalized mouse embryonic fibroblasts (MEFs) in the regulation of cell division, microtubules, ciliogenesis, and mitochondrial fusion. Here, using similar strategies with the paralogues ELMOD1 and ELMOD3, we identify novel functions and locations of these cell regulators and compare them to those of ELMOD2, allowing the determination of functional redundancy among the family members. We found strong similarities in phenotypes resulting from deletion of either <i>Elmod1</i> or <i>Elmod3</i> and marked differences from those arising in <i>Elmod2</i> deletion lines. Deletion of either <i>Elmod1</i> or <i>Elmod3</i> results in the decreased ability of cells to form primary cilia, loss of a subset of proteins from cilia, and accumulation of some ciliary proteins at the Golgi, predicted to result from compromised traffic from the Golgi to cilia. These phenotypes are reversed upon activating mutant expression of either ARL3 or ARL16, linking their roles to ELMOD1/3 actions.
Addresses
  • Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322.
Autoren
  • Rachel E Turn
  • Yihan Hu
  • Skylar I Dewees
  • Narra Devi
  • Michael P East
  • Katherine R Hardin
  • Tala Khatib
  • Joshua Linnert
  • Uwe Wolfrum
  • Michael J Lim
  • James E Casanova
  • Tamara Caspary
  • Richard A Kahn
DOI
10.1091/mbc.e21-09-0443
eISSN
1939-4586
Externe Identifier
  • PubMed Identifier: 34818063
  • PubMed Central ID: PMC9236152
Funding acknowledgements
  • NIGMS NIH HHS: R01 GM127361
  • NIGMS NIH HHS: R01 GM110663
  • NIGMS NIH HHS: R35 GM122568
  • NIGMS NIH HHS: R35 GM122549
  • NCI NIH HHS: F31 CA236493
  • NICHD NIH HHS: F31 HD096815
Open access
true
ISSN
1059-1524
Ausgabe der Veröffentlichung
2
Zeitschrift
Molecular biology of the cell
Schlüsselwörter
  • Cilia
  • Microtubules
  • Golgi Apparatus
  • Fibroblasts
  • Animals
  • Mice
  • ADP-Ribosylation Factors
  • GTPase-Activating Proteins
  • Cytoskeletal Proteins
  • Signal Transduction
  • Mitochondrial Dynamics
Sprache
eng
Medium
Print-Electronic
Online publication date
2021
Open access status
Open Access
Paginierung
ar13
Datum der Veröffentlichung
2022
Status
Published
Publisher licence
CC BY-NC-SA
Datum der Datenerfassung
2021
Titel
The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic.
Sub types
  • Research Support, Non-U.S. Gov't
  • research-article
  • Journal Article
  • Research Support, N.I.H., Extramural
Ausgabe der Zeitschrift
33

Files

https://europepmc.org/articles/PMC9236152?pdf=render

Data source: Europe PubMed Central

Abstract
ELMODs are a family of three mammalian paralogues that display GTPase-activating protein (GAP) activity toward a uniquely broad array of ADP-ribosylation factor (ARF) family GTPases that includes ARF-like (ARL) proteins. ELMODs are ubiquitously expressed in mammalian tissues, highly conserved across eukaryotes, and ancient in origin, being present in the last eukaryotic common ancestor. We described functions of ELMOD2 in immortalized mouse embryonic fibroblasts (MEFs) in the regulation of cell division, microtubules, ciliogenesis, and mitochondrial fusion. Here, using similar strategies with the paralogues ELMOD1 and ELMOD3, we identify novel functions and locations of these cell regulators and compare them to those of ELMOD2, allowing the determination of functional redundancy among the family members. We found strong similarities in phenotypes resulting from deletion of either Elmod1 or Elmod3 and marked differences from those arising in Elmod2 deletion lines. Deletion of either Elmod1 or Elmod3 results in the decreased ability of cells to form primary cilia, loss of a subset of proteins from cilia, and accumulation of some ciliary proteins at the Golgi, predicted to result from compromised traffic from the Golgi to cilia. These phenotypes are reversed upon activating mutant expression of either ARL3 or ARL16, linking their roles to ELMOD1/3 actions.
Autoren
  • Rachel E Turn
  • Yihan Hu
  • Skylar I Dewees
  • Narra Devi
  • Michael P East
  • Katherine R Hardin
  • Tala Khatib
  • Joshua Linnert
  • Uwe Wolfrum
  • Michael J Lim
  • James E Casanova
  • Tamara Caspary
  • Richard A Kahn
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/34818063
DOI
10.1091/mbc.E21-09-0443
eISSN
1939-4586
Externe Identifier
  • PubMed Central ID: PMC9236152
Funding acknowledgements
  • NIGMS NIH HHS: R35 GM122568
  • NICHD NIH HHS: F31 HD096815
  • NIGMS NIH HHS: R35 GM122549
  • NIGMS NIH HHS: R01 GM110663
  • NCI NIH HHS: F31 CA236493
  • NIGMS NIH HHS: R01 GM127361
Ausgabe der Veröffentlichung
2
Zeitschrift
Mol Biol Cell
Schlüsselwörter
  • ADP-Ribosylation Factors
  • Animals
  • Cilia
  • Cytoskeletal Proteins
  • Fibroblasts
  • GTPase-Activating Proteins
  • Golgi Apparatus
  • Mice
  • Microtubules
  • Mitochondrial Dynamics
  • Signal Transduction
Sprache
eng
Country
United States
Paginierung
ar13
Datum der Veröffentlichung
2022
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2022
Titel
The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic.
Sub types
  • Journal Article
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
33

Data source: PubMed

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