Evidence map›Paper›PMID 29311115›Full record

ArticleThe EMBO journal2018

Miro proteins coordinate microtubule- and actin-dependent mitochondrial transport and distribution.

Guillermo López-Doménech, Christian Covill-Cooke, Davor Ivankovic, Els F Halff, David F Sheehan, Rosalind Norkett, Nicol Birsa, Josef T Kittler

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
217citing papers in PubMed, 1 pooled it
12.7field-weighted citation impact, top 1% 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

217 citing papers in PubMed, 1 synthesis or guideline pooled it, 332 citations in OpenAlex.

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  18. Control of microglial dynamics by the Arp2/3 complex and the autism- and schizophrenia-associated protein CYFIP1.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  19. Review
  20. Review

157 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Guillermo López-DoménechDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.ORCID 0000-0002-3114-2082
Christian Covill-CookeDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
Davor IvankovicDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
Els F HalffDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
David F SheehanDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
Rosalind NorkettDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
Nicol BirsaDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
Josef T KittlerDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK j.kittler@ucl.ac.uk.ORCID 0000-0002-3437-9456
University College London · GB

Funding

European Research Council 282430Medical Research Council 1368635
6 · The paper itself

Abstract

In the current model of mitochondrial trafficking, Miro1 and Miro2 Rho-GTPases regulate mitochondrial transport along microtubules by linking mitochondria to kinesin and dynein motors. By generating Miro1/2 double-knockout mouse embryos and single- and double-knockout embryonic fibroblasts, we demonstrate the essential and non-redundant roles of Miro proteins for embryonic development and subcellular mitochondrial distribution. Unexpectedly, the TRAK1 and TRAK2 motor protein adaptors can still localise to the outer mitochondrial membrane to drive anterograde mitochondrial motility in Miro1/2 double-knockout cells. In contrast, we show that TRAK2-mediated retrograde mitochondrial transport is Miro1-dependent. Interestingly, we find that Miro is critical for recruiting and stabilising the mitochondrial myosin Myo19 on the mitochondria for coupling mitochondria to the actin cytoskeleton. Moreover, Miro depletion during PINK1/Parkin-dependent mitophagy can also drive a loss of mitochondrial Myo19 upon mitochondrial damage. Finally, aberrant positioning of mitochondria in Miro1/2 double-knockout cells leads to disruption of correct mitochondrial segregation during mitosis. Thus, Miro proteins can fine-tune actin- and tubulin-dependent mitochondrial motility and positioning, to regulate key cellular functions such as cell proliferation.

Indexed as

ActinsAdaptor Proteins, Vesicular TransportAnimalsBiological TransportCarrier ProteinsCell Line, TransformedCell ProliferationDyneinsEmbryonic DevelopmentKinesinsMiceMice, KnockoutMicrotubulesMitochondriaMitochondrial MembranesMitochondrial ProteinsActinsAdaptor Proteins, Vesicular TransportCarrier ProteinsDyneinsKinesinsMiro-1 protein, mouseMitochondrial ProteinsMyo19 protein, mouseMyosinsNerve Tissue Proteinsparkin proteinProtein KinasesPTEN-Induced Putative Kinaserho GTP-Binding ProteinsRhot2 protein, mouseTrak1 protein, mouseTRAK2 protein, mouseUbiquitin-Protein Ligasesmicropatternmitofusinmyosin XIXRhot1Rhot2

Identifiers

PMID29311115
PMCPMC5793800
OpenAlexW2783417803

What OpenQuestion 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 OpenQuestion graph.