Evidence map›Paper›PMID 26076409›Full record

ArticleeLife2015

Deletion of a kinesin I motor unmasks a mechanism of homeostatic branching control by neurotrophin-3.

Thomas O Auer, Tong Xiao, Valerie Bercier, Christoph Gebhardt, Karine Duroure, Jean-Paul Concordet, Claire Wyart, Maximiliano Suster, Koichi Kawakami, Joachim Wittbrodt and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Frontiers in neuroscience · 2019
    Pooled it
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  15. Zebrafish as a Model for the Study of LiveFrontiers in cell and developmental biology · 2019
    Article
  16. Regulation of long-distance transport of mitochondria along microtubules.Cellular and molecular life sciences : CMLS · 2018
    Review
  17. Article
  18. Article
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  20. Review
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

12 authors at 4 institutions in 5 countries.

Thomas O AuerInstitut Curie, Centre de Recherche, Paris, France.
Tong XiaoDepartment of Physiology, University of California San Francisco, San Francisco, United States.
Valerie BercierInstitut Curie, Centre de Recherche, Paris, France.
Christoph GebhardtInstitut Curie, Centre de Recherche, Paris, France.
Karine DuroureInstitut Curie, Centre de Recherche, Paris, France.
Jean-Paul ConcordetMuséum National d'Histoire naturelle, Inserm U 1154, CNRS, UMR 7196, Muséum National d'Histoire Naturelle, Paris, France.
Claire WyartInstitut du Cerveau et de la Moelle épinière, ICM, Inserm U 1127, CNRS, UMR 7225, Sorbonne Universités, UPMC University Paris 6, Paris, France.
Maximiliano SusterNeural Circuits and Behaviour Group, Uni Research AS High Technology Centre, Bergen, Norway.
Koichi KawakamiDivision of Molecular and Developmental Biology, National Institute of Genetics, Shizuoka, Japan.
Joachim WittbrodtCentre for Organismal Studies, University of Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-8550-7377
Herwig BaierDepartment of Physiology, University of California San Francisco, San Francisco, United States.
Filippo Del BeneInstitut Curie, Centre de Recherche, Paris, France.ORCID http://orcid.org/0000-0001-8551-2846
Centre National de la Recherche Scientifique · FRNational Institute of Genetics · JPUniversity of California, San Francisco · USHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development and function of highly polarized cells such as neurons depend on microtubule-associated intracellular transport, but little is known about contributions of specific molecular motors to the establishment of synaptic connections. In this study, we investigated the function of the Kinesin I heavy chain Kif5aa during retinotectal circuit formation in zebrafish. Targeted disruption of Kif5aa does not affect retinal ganglion cell differentiation, and retinal axons reach their topographically correct targets in the tectum, albeit with a delay. In vivo dynamic imaging showed that anterograde transport of mitochondria is impaired, as is synaptic transmission. Strikingly, disruption of presynaptic activity elicits upregulation of Neurotrophin-3 (Ntf3) in postsynaptic tectal cells. This in turn promotes exuberant branching of retinal axons by signaling through the TrkC receptor (Ntrk3). Thus, our study has uncovered an activity-dependent, retrograde signaling pathway that homeostatically controls axonal branching.

Indexed as

AnimalsAnimals, Genetically ModifiedAxonsBiological TransportBlotting, WesternCell PolarityChromosome MappingCloning, MolecularDNA PrimersGenotypeImmunohistochemistryIn Situ HybridizationKinesinsMicroscopy, ConfocalMicroscopy, Electron, TransmissionMitochondriaDNA PrimersKif5aa protein, zebrafishKinesinsNeurotrophin 3Zebrafish Proteinsaxonal developmentneuroscienceneurotrophic signalingvisual systemzebrafish

Identifiers

PMID26076409
PMCPMC4467164
OpenAlexW1930489890

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.