The small GTPase Arf1 modulates mitochondrial morphology and function.
- Ackema KB Growth and Development, Biozentrum University of Basel, Basel, Switzerland.
- Hench J Division of Neuropathology, Institute of Pathology, University Hospital Basel, Basel, Switzerland.
- Böckler S Cell Biology, University of Bayreuth, Bayreuth, Germany.
- Wang SC Institute for Molecular and Cell Biology, Singapore City, Singapore.
- Sauder U Microscopy Center, Biozentrum University of Basel, Basel, Switzerland.
- Mergentaler H Growth and Development, Biozentrum University of Basel, Basel, Switzerland.
- Westermann B Cell Biology, University of Bayreuth, Bayreuth, Germany.
- Bard F Institute for Molecular and Cell Biology, Singapore City, Singapore.
- Frank S Division of Neuropathology, Institute of Pathology, University Hospital Basel, Basel, Switzerland.
- Spang A Growth and Development, Biozentrum University of Basel, Basel, Switzerland anne.spang@unibas.ch.
- 2014-09-06
Published in:
- The EMBO journal. - 2014
Cdc48
ER–mitochondrial contact sites
mitochondria‐associated degradation
mitophagy
stress response
ADP-Ribosylation Factor 1
Animals
Caenorhabditis elegans
Caenorhabditis elegans Proteins
GTP Phosphohydrolases
Membrane Proteins
Mitochondria
Mitochondrial Membranes
Mitochondrial Proteins
Saccharomyces cerevisiae
Saccharomyces cerevisiae Proteins
English
The small GTPase Arf1 plays critical roles in membrane traffic by initiating the recruitment of coat proteins and by modulating the activity of lipid-modifying enzymes. Here, we report an unexpected but evolutionarily conserved role for Arf1 and the ArfGEF GBF1 at mitochondria. Loss of function of ARF-1 or GBF-1 impaired mitochondrial morphology and activity in Caenorhabditis elegans. Similarly, mitochondrial defects were observed in mammalian and yeast cells. In Saccharomyces cerevisiae, aberrant clusters of the mitofusin Fzo1 accumulated in arf1-11 mutants and were resolved by overexpression of Cdc48, an AAA-ATPase involved in ER and mitochondria-associated degradation processes. Yeast Arf1 co-fractionated with ER and mitochondrial membranes and interacted genetically with the contact site component Gem1. Furthermore, similar mitochondrial abnormalities resulted from knockdown of either GBF-1 or contact site components in worms, suggesting that the role of Arf1 in mitochondrial functioning is linked to ER-mitochondrial contacts. Thus, Arf1 is involved in mitochondrial homeostasis and dynamics, independent of its role in vesicular traffic.
- Language
-
- English
- Open access status
- green
- Identifiers
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- DOI 10.15252/embj.201489039
- PMID 25190516
- Persistent URL
- https://sonar.ch/global/documents/201722
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