Evidence map›Paper›PMID 25190516›Full record

ArticleThe EMBO journal2014

The small GTPase Arf1 modulates mitochondrial morphology and function.

Karin B Ackema, Jürgen Hench, Stefan Böckler, Shyi Chyi Wang, Ursula Sauder, Heidi Mergentaler, Benedikt Westermann, Frédéric Bard, Stephan Frank, Anne Spang

Abstract read
In one paragraph

Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 97 citations in OpenAlex.

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  11. Arfs on the Golgi: four conductors, one orchestra.Frontiers in molecular biosciences · 2025
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Karin B AckemaGrowth and Development, Biozentrum University of Basel, Basel, Switzerland.
Jürgen HenchDivision of Neuropathology, Institute of Pathology, University Hospital Basel, Basel, Switzerland.
Stefan BöcklerCell Biology, University of Bayreuth, Bayreuth, Germany.
Shyi Chyi WangInstitute for Molecular and Cell Biology, Singapore City, Singapore.
Ursula SauderMicroscopy Center, Biozentrum University of Basel, Basel, Switzerland.
Heidi MergentalerGrowth and Development, Biozentrum University of Basel, Basel, Switzerland.
Benedikt WestermannCell Biology, University of Bayreuth, Bayreuth, Germany.
Frédéric BardInstitute for Molecular and Cell Biology, Singapore City, Singapore.
Stephan FrankDivision of Neuropathology, Institute of Pathology, University Hospital Basel, Basel, Switzerland.
Anne SpangGrowth and Development, Biozentrum University of Basel, Basel, Switzerland anne.spang@unibas.ch.
University of Basel · CHInstitute of Molecular and Cell Biology · SGUniversity Hospital of Basel · CHUniversity of Bayreuth · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

ADP-Ribosylation Factor 1AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGTP PhosphohydrolasesMembrane ProteinsMitochondriaMitochondrial MembranesMitochondrial ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsADP-Ribosylation Factor 1Caenorhabditis elegans ProteinsFZO1 protein, S cerevisiaeGEM1 protein, S cerevisiaeGTP PhosphohydrolasesMembrane ProteinsMitochondrial ProteinsSaccharomyces cerevisiae ProteinsCdc48ER–mitochondrial contact sitesmitochondria‐associated degradationmitophagystress response

Identifiers

PMID25190516
PMCPMC4282574
OpenAlexW2112940226

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.