Evidence map›Paper›PMID 33771901›Full record

ArticleeNeuro

FEZ1 Forms Complexes with CRMP1 and DCC to Regulate Axon and Dendrite Development.

Jie Yin Chua, Shi Jun Ng, Oleksandr Yagensky, Erich E Wanker, John Jia En Chua

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Expression of the schizophrenia associated geneFrontiers in neuroscience · 2023
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  8. Review
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  10. Transsynaptic cerebellin 4-neogenin 1 signaling mediates LTP in the mouse dentate gyrus.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

5 authors at 4 institutions in 2 countries.

Jie Yin ChuaDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.
Shi Jun NgDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.
Oleksandr YagenskyDepartment of Neurobiology, Max Planck Institute for Biophysical Chemistry, Göttingen 37077, Germany.
Erich E WankerMax Delbrück Center for Molecular Medicine, Berlin-Buch 13092, Germany.ORCID 0000-0001-8072-1630
John Jia En ChuaDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore phsjcje@nus.edu.sg.ORCID 0000-0002-5615-1014
Agency for Science, Technology and Research · SGMax Delbrück Center · DEMax Planck Institute for Biophysical Chemistry · DENational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elaboration of neuronal processes is an early step in neuronal development. Guidance cues must work closely with intracellular trafficking pathways to direct expanding axons and dendrites to their target neurons during the formation of neuronal networks. However, how such coordination is achieved remains incompletely understood. Here, we characterize an interaction between fasciculation and elongation protein zeta 1 (FEZ1), an adapter involved in synaptic protein transport, and collapsin response mediator protein (CRMP)1, a protein that functions in growth cone guidance, at neuronal growth cones. We show that similar to CRMP1 loss-of-function mutants, FEZ1 deficiency in rat hippocampal neurons causes growth cone collapse and impairs axonal development. Strikingly, FEZ1-deficient neurons also exhibited a reduction in dendritic complexity stronger than that observed in CRMP1-deficient neurons, suggesting that the former could partake in additional developmental signaling pathways. Supporting this, FEZ1 colocalizes with VAMP2 in developing hippocampal neurons and forms a separate complex with deleted in colorectal cancer (DCC) and Syntaxin-1 (Stx1), components of the Netrin-1 signaling pathway that are also involved in regulating axon and dendrite development. Significantly, developing axons and dendrites of FEZ1-deficient neurons fail to respond to Netrin-1 or Netrin-1 and Sema3A treatment, respectively. Taken together, these findings highlight the importance of FEZ1 as a common effector to integrate guidance signaling pathways with intracellular trafficking to mediate axo-dendrite development during neuronal network formation.

Indexed as

AxonsReceptors, Cell SurfaceAdaptor Proteins, Signal TransducingAnimalsDCC ReceptorGrowth ConesNerve Tissue ProteinsNeuronsRatsAdaptor Proteins, Signal TransducingDcc protein, ratDCC ReceptorFez1 protein, ratNerve Tissue ProteinsReceptors, Cell SurfaceaxonCRMP1DCCdendritedevelopmentFEZ1

Identifiers

PMID33771901
PMCPMC8174033
OpenAlexW3137149476

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.