Evidence map›Paper›PMID 38514619›Full record

ArticleNature communications2024

The AMPK-related kinase NUAK1 controls cortical axons branching by locally modulating mitochondrial metabolic functions.

Marine Lanfranchi, Sozerko Yandiev, Géraldine Meyer-Dilhet, Salma Ellouze, Martijn Kerkhofs, Raphael Dos Reis, Audrey Garcia, Camille Blondet, Alizée Amar, Anita Kneppers and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  11. Chasing the Ghost Proteome in the Dark Matter.Molecular & cellular proteomics : MCP · 2025
    Review
  12. Mitochondrial Microproteins: Emerging Regulators in Neurodevelopment and Neurodegeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.bioRxiv : the preprint server for biology · 2025
    Article
  18. NUAK: never underestimate a kinase.Essays in biochemistry · 2024
    Review
  19. Review
  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

20 authors at 3 institutions in 2 countries.

Marine Lanfranchi *Univ Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Sozerko Yandiev *Univ Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Géraldine Meyer-DilhetUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Salma EllouzeUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Martijn KerkhofsUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Raphael Dos ReisUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Audrey GarciaUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Camille BlondetUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Alizée AmarUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Anita KneppersUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.ORCID http://orcid.org/0000-0003-4901-5468
Hélène PolvècheLaboratoire de Biologie et Modelisation de la Cellule, Ecole Normale Superieure de Lyon, CNRS, UMR 5239, Inserm, U1293, Universite Claude Bernard Lyon 1, 46 allée d'Italie F-69364, Lyon, France.
Damien PlassardCNRS UMR 7104, INSERM U1258, GenomEast Platform, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg, Illkirch, France.ORCID http://orcid.org/0000-0001-8569-6163
Marc ForetzUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.ORCID http://orcid.org/0000-0001-7017-9032
Benoit ViolletUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.ORCID http://orcid.org/0000-0002-0121-0224
Kei SakamotoNovo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, 2200, Denmark.ORCID http://orcid.org/0000-0001-8839-5980
Rémi MounierUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Cyril F BourgeoisLaboratoire de Biologie et Modelisation de la Cellule, Ecole Normale Superieure de Lyon, CNRS, UMR 5239, Inserm, U1293, Universite Claude Bernard Lyon 1, 46 allée d'Italie F-69364, Lyon, France.ORCID http://orcid.org/0000-0002-0756-5501
Olivier RaineteauUniv Lyon, Université Claude Bernard Lyon 1, Inserm, Stem Cell and Brain Research Institute U1208, 69500, Bron, France.
Evelyne GoillotUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France.
Julien CourchetUniv Lyon, Université Claude Bernard Lyon 1, CNRS, Inserm, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, U1315, Institut NeuroMyoGène, 69008, Lyon, France. julien.courchet@univ-lyon1.fr.ORCID http://orcid.org/0000-0002-1199-9329
Université Claude Bernard Lyon 1 · FRCentre National de la Recherche Scientifique · FRUniversity of Copenhagen · DK

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-10-INBS-0009Agence Nationale de la Recherche (French National Research Agency) ANR-11-IDEX-0007Agence Nationale de la Recherche (French National Research Agency) ANR-11-LABX-0042EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC-STG-678302-NEUROMETFondation pour la Recherche Médicale (Foundation for Medical Research in France) AJE20141031276Fondation pour la Recherche Médicale (Foundation for Medical Research in France) SPF202110014126Novo Nordisk Fonden (Novo Nordisk Foundation) NNF18CC0034900
6 · The paper itself

Abstract

The cellular mechanisms underlying axonal morphogenesis are essential to the formation of functional neuronal networks. We previously identified the autism-linked kinase NUAK1 as a central regulator of axon branching through the control of mitochondria trafficking. However, (1) the relationship between mitochondrial position, function and axon branching and (2) the downstream effectors whereby NUAK1 regulates axon branching remain unknown. Here, we report that mitochondria recruitment to synaptic boutons supports collateral branches stabilization rather than formation in mouse cortical neurons. NUAK1 deficiency significantly impairs mitochondrial metabolism and axonal ATP concentration, and upregulation of mitochondrial function is sufficient to rescue axonal branching in NUAK1 null neurons in vitro and in vivo. Finally, we found that NUAK1 regulates axon branching through the mitochondria-targeted microprotein BRAWNIN. Our results demonstrate that NUAK1 exerts a dual function during axon branching through its ability to control mitochondrial distribution and metabolic activity.

Indexed as

AMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsAxonsMiceMitochondriaNeuronsProtein KinasesRepressor ProteinsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesNUAK1 protein, mouseProtein KinasesRepressor Proteins

Identifiers

PMID38514619
PMCPMC10958033
OpenAlexW4393055434

What OpenQuestion holds

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Registered trials

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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.