Evidence map›Paper›PMID 25653356›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Linking cell surface receptors to microtubules: tubulin folding cofactor D mediates Dscam functions during neuronal morphogenesis.

Misako Okumura, Chisako Sakuma, Masayuki Miura, Takahiro Chihara

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  4. A Variant inInternational journal of molecular sciences · 2023
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  13. DSCAM-mediated control of dendritic and axonal arbor outgrowth enforces tiling and inhibits synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2017
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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

4 authors at 2 institutions in 1 country.

Misako OkumuraDepartment of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan, and.
Chisako SakumaDepartment of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan, and.
Masayuki MiuraDepartment of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan, and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo, 102-0076, Japan.
Takahiro ChiharaDepartment of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan, and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo, 102-0076, Japan tchihara@mol.f.u-tokyo.ac.jp.
The University of Tokyo · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Formation of functional neural networks requires the coordination of cell surface receptors and downstream signaling cascades, which eventually leads to dynamic remodeling of the cytoskeleton. Although a number of guidance receptors affecting actin cytoskeleton remodeling have been identified, it is relatively unknown how microtubule dynamics are regulated by guidance receptors. We used Drosophila olfactory projection neurons to study the molecular mechanisms of neuronal morphogenesis. Dendrites of each projection neuron target a single glomerulus of ∼50 glomeruli in the antennal lobe, and the axons show stereotypical pattern of terminal arborization. In the course of genetic analysis of the dachsous mutant allele (ds(UAO71)), we identified a mutation in the tubulin folding cofactor D gene (TBCD) as a background mutation. TBCD is one of five tubulin-folding cofactors required for the formation of α- and β-tubulin heterodimers. Single-cell clones of projection neurons homozygous for the TBCD mutation displayed disruption of microtubules, resulting in ectopic arborization of dendrites, and axon degeneration. Interestingly, overexpression of TBCD also resulted in microtubule disruption and ectopic dendrite arborization, suggesting that an optimum level of TBCD is crucial for in vivo neuronal morphogenesis. We further found that TBCD physically interacts with the intracellular domain of Down syndrome cell adhesion molecule (Dscam), which is important for neural development and has been implicated in Down syndrome. Genetic analyses revealed that TBCD cooperates with Dscam in vivo. Our study may offer new insights into the molecular mechanism underlying the altered neural networks in cognitive disabilities of Down syndrome.

Indexed as

NeurogenesisAmino Acid SequenceAnimalsAxonsBinding SitesCell Adhesion MoleculesCells, CulturedDendritesDrosophilaDrosophila ProteinsMicrotubule-Associated ProteinsMicrotubulesMolecular Sequence DataProtein BindingSensory Receptor CellsCell Adhesion MoleculesDrosophila ProteinsDscam1 protein, DrosophilaMicrotubule-Associated ProteinsTBCD protein, DrosophilaaxondendriteDrosophilaDscammicrotubuletubulin

Identifiers

PMID25653356
PMCPMC6705359
OpenAlexW2094173900

What OpenQuestion holds

Textmetadata
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.