Evidence map›Paper›PMID 28981113›Full record

ArticleCell death & disease2017

Cofilin1-dependent actin dynamics control DRP1-mediated mitochondrial fission.

Katharina Rehklau, Lena Hoffmann, Christine B Gurniak, Martin Ott, Walter Witke, Luca Scorrano, Carsten Culmsee, Marco B Rust

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

58 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Article
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  8. Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. The multiple links between actin and mitochondria.Nature reviews. Molecular cell biology · 2023
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 4 countries.

Katharina RehklauNeurobiology/Neurophysiology Group, University of Kaiserslautern, Kaiserslautern, Germany.
Lena HoffmannInstitute for Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.
Christine B GurniakInstitute of Genetics, University of Bonn, Bonn, Germany.
Martin OttInstitute for Biochemistry and Biophysics, University of Stockholm, Stockholm, Sweden.
Walter WitkeInstitute of Genetics, University of Bonn, Bonn, Germany.
Luca ScorranoDepartment of Biology, University of Padua, Padua, Italy.
Carsten CulmseeInstitute for Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany.ORCID 0000-0002-5121-5015
Marco B RustNeurobiology/Neurophysiology Group, University of Kaiserslautern, Kaiserslautern, Germany.
Philipps University of Marburg · DEUniversity of Bonn · DEUniversity of Kaiserslautern · DEStockholm University · SEUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria form highly dynamic networks in which organelles constantly fuse and divide. The relevance of mitochondrial dynamics is evident from its implication in various human pathologies, including cancer or neurodegenerative, endocrine and cardiovascular diseases. Dynamin-related protein 1 (DRP1) is a key regulator of mitochondrial fission that oligomerizes at the mitochondrial outer membrane and hydrolyzes GTP to drive mitochondrial fragmentation. Previous studies demonstrated that DRP1 recruitment and mitochondrial fission is promoted by actin polymerization at the mitochondrial surface, controlled by the actin regulatory proteins inverted formin 2 (INF2) and Spire1C. These studies suggested the requirement of additional actin regulatory activities to control DRP1-mediated mitochondrial fission. Here we show that the actin-depolymerizing protein cofilin1, but not its close homolog actin-depolymerizing factor (ADF), is required to maintain mitochondrial morphology. Deletion of cofilin1 caused mitochondrial DRP1 accumulation and fragmentation, without altering mitochondrial function or other organelles' morphology. Mitochondrial morphology in cofilin1-deficient cells was restored upon (i) re-expression of wild-type cofilin1 or a constitutively active mutant, but not of an actin-binding-deficient mutant, (ii) pharmacological destabilization of actin filaments and (iii) genetic depletion of DRP1. Our work unraveled a novel function for cofilin1-dependent actin dynamics in mitochondrial fission, and identified cofilin1 as a negative regulator of mitochondrial DRP1 activity. We conclude that cofilin1 is required for local actin dynamics at mitochondria, where it may balance INF2/Spire1C-induced actin polymerization.

Indexed as

Actin CytoskeletonActinsAnimalsCells, CulturedCofilin 1Death-Associated Protein KinasesDestrinFibroblastsForminsHumansMiceMicrofilament ProteinsMitochondriaMitochondrial DynamicsNerve Tissue ProteinsProtein BindingActinsCofilin 1Death-Associated Protein KinasesDestrinForminsINF2 protein, mouseMicrofilament ProteinsNerve Tissue ProteinsSpire1 protein, mouse

Identifiers

PMID28981113
PMCPMC5680571
OpenAlexW2762321925

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.