Evidence map›Paper›PMID 20300184›Full record

ArticlePloS one2010

Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.

Renee Baran, Liliana Castelblanco, Garland Tang, Ian Shapiro, Alexandr Goncharov, Yishi Jin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The Expression and Function of Tubulin Isotypes inFrontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. The Claudin-like Protein HPO-30 Is Required to Maintain LAChRs at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 3 institutions in 1 country.

Renee BaranBiology Department, Occidental College, Los Angeles, California, United States of America.
Liliana Castelblanco
Garland Tang
Ian Shapiro
Alexandr Goncharov
Yishi Jin
Occidental College · USHoward Hughes Medical Institute · USUniversity of California, San Diego · US

Funding

GABAERGIC NEURON DIFFERENTIATION IN C ELEGANSR01NS035546 · NINDS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI JIN, YISHI · 1996 to 2016
$5.3M
GABAergic Neuron Differentiation in C.elegansR37NS035546 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JIN, YISHI · 2017 to 2021
$2.4M
Howard Hughes Medical InstituteNINDS NIH HHS NS35546NINDS NIH HHS R01 NS035546NINDS NIH HHS R37 NS035546
6 · The paper itself

Abstract

Regulation of microtubule dynamics underlies many fundamental cellular mechanisms including cell division, cell motility, and transport. In neurons, microtubules play key roles in cell migration, axon outgrowth, control of axon and synapse growth, and the regulated transport of vesicles and structural components of synapses. Loss of synapse and axon integrity and disruption of axon transport characterize many neurodegenerative diseases. Recently, mutations that specifically alter the assembly or stability of microtubules have been found to directly cause neurodevelopmental defects or neurodegeneration in vertebrates. We report here the characterization of a missense mutation in the C-terminal domain of C. elegans alpha-tubulin, tba-1(ju89), that disrupts motor neuron synapse and axon development. Mutant ju89 animals exhibit reduction in the number and size of neuromuscular synapses, altered locomotion, and defects in axon extension. Although null mutations of tba-1 show a nearly wild-type pattern, similar axon outgrowth defects were observed in animals lacking the beta-tubulin TBB-2. Genetic analysis reveals that tba-1(ju89) affects synapse development independent of its role in axon outgrowth. tba-1(ju89) is an altered function allele that most likely perturbs interactions between TBA-1 and specific microtubule-associated proteins that control microtubule dynamics and transport of components needed for synapse and axon growth.

Indexed as

AllelesAmino Acid SequenceAnimalsAxonsCaenorhabditis elegansGreen Fluorescent ProteinsMicrotubulesMolecular Sequence DataMotor NeuronsMutation, MissenseProtein Structure, TertiarySequence Homology, Amino AcidSynapsesTubulinGreen Fluorescent ProteinsTubulin

Identifiers

PMID20300184
PMCPMC2836382
OpenAlexW2037196594

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.