Evidence map›Paper›PMID 36367943›Full record

ArticleScience advances2022

AMPK-dependent phosphorylation of MTFR1L regulates mitochondrial morphology.

Lisa Tilokani, Fiona M Russell, Stevie Hamilton, Daniel M Virga, Mayuko Segawa, Vincent Paupe, Anja V Gruszczyk, Margherita Protasoni, Luis-Carlos Tabara, Mark Johnson and 5 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
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  8. MTFR1L is a cardiac antiaging factor for maintenance of mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Review
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  14. The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025
    Review
  15. Article
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  17. Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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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

15 authors at 4 institutions in 2 countries.

Lisa TilokaniMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0003-1228-6985
Fiona M RussellDivision of Cell Signalling & Immunology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.ORCID 0000-0003-4995-2734
Stevie HamiltonDepartment of Neuroscience, Columbia University, New York, NY 10032, USA.
Daniel M VirgaDepartment of Neuroscience, Columbia University, New York, NY 10032, USA.ORCID 0000-0002-7248-3596
Mayuko SegawaMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0002-5680-9576
Vincent PaupeMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.
Anja V GruszczykMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0003-3060-4107
Margherita ProtasoniMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0001-6557-461X
Luis-Carlos TabaraMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.
Mark JohnsonMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.
Hanish AnandMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0002-3850-9641
Michael P MurphyMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0003-1115-9618
D Grahame HardieDivision of Cell Signalling & Immunology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.ORCID 0000-0002-8373-7379
Franck PolleuxDepartment of Neuroscience, Columbia University, New York, NY 10032, USA.ORCID 0000-0003-4313-0481
Julien PrudentMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Hills Road, CB2 0XY Cambridge, UK.ORCID 0000-0003-3821-6088
MRC Mitochondrial Biology Unit · GBColumbia University · USUniversity of Dundee · GBUniversity of Cambridge · GB

Funding

Development, Maintenance, and Human-Specific Evolution of Cortical CircuitsR35NS127232 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FRANCK POLLEUX · 2022 to 2026
$6.1M
Role of ER-mitochondria contacts in dendritic Ca2+ homeostasis, synaptic integration and circuit functionR01NS107483 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI POLLEUX, FRANCK · 2019 to 2021
$1.6M
Medical Research Council MC_UU_00015/7Medical Research Council MC_UU_00028/5NINDS NIH HHS R01 NS107483NINDS NIH HHS R35 NS127232Wellcome Trust
6 · The paper itself

Abstract

Mitochondria are dynamic organelles that undergo membrane remodeling events in response to metabolic alterations to generate an adequate mitochondrial network. Here, we investigated the function of mitochondrial fission regulator 1-like protein (MTFR1L), an uncharacterized protein that has been identified in phosphoproteomic screens as a potential AMP-activated protein kinase (AMPK) substrate. We showed that MTFR1L is an outer mitochondrial membrane-localized protein modulating mitochondrial morphology. Loss of MTFR1L led to mitochondrial elongation associated with increased mitochondrial fusion events and levels of the mitochondrial fusion protein, optic atrophy 1. Mechanistically, we show that MTFR1L is phosphorylated by AMPK, which thereby controls the function of MTFR1L in regulating mitochondrial morphology both in mammalian cell lines and in murine cortical neurons in vivo. Furthermore, we demonstrate that MTFR1L is required for stress-induced AMPK-dependent mitochondrial fragmentation. Together, these findings identify MTFR1L as a critical mitochondrial protein transducing AMPK-dependent metabolic changes through regulation of mitochondrial dynamics.

Indexed as

AMP-Activated Protein KinasesMitochondrial DynamicsAnimalsMammalsMembrane ProteinsMiceMitochondriaMitochondrial ProteinsPhosphorylationAMP-Activated Protein KinasesMembrane ProteinsMitochondrial Proteins

Identifiers

PMID36367943
PMCPMC9651865
OpenAlexW4308916364

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.