Evidence map›Paper›PMID 17881523›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Tomosyn negatively regulates CAPS-dependent peptide release at Caenorhabditis elegans synapses.

Elena O Gracheva, Anna O Burdina, Denis Touroutine, Martine Berthelot-Grosjean, Hetal Parekh, Janet E Richmond

Erratum issuedOpen access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.3field-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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  8. Conditional Degradation of UNC-31/CAPS Enables Spatiotemporal Analysis of Neuropeptide Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  9. Article
  10. ENPL-1, theDevelopment (Cambridge, England) · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Dynamic Partitioning of Synaptic Vesicle Pools by the SNARE-Binding Protein Tomosyn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  15. NLP-12 engages different UNC-13 proteins to potentiate tonic and evoked release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  16. Article
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  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Elena O GrachevaDepartment of Biological Sciences, Science and Engineering Labs, University of Illinois at Chicago, Chicago, Illinois 60607, USA.
Anna O Burdina
Denis Touroutine
Martine Berthelot-Grosjean
Hetal Parekh
Janet E Richmond
University of Illinois Chicago · US

Funding

The role of tomosyn in synaptic transmission.R01MH073156 · NIMH · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RICHMOND, JANET E · 2006 to 2010
$2.0M
UNC-18 function in C. elegans synaptic transmissionR01NS041477 · NINDS · UNIVERSITY OF UTAH · PI RICHMOND, JANET E · 2002 to 2006
$1.2M
NIMH NIH HHS R01 MH073156NINDS NIH HHS R01 NS041477
6 · The paper itself

Abstract

The syntaxin-interacting protein tomosyn is thought to be a key regulator of exocytosis, although its precise mechanism of action has yet to be elucidated. Here we examined the role of tomosyn in peptide secretion in Caenorhabditis elegans tomosyn (tom-1) mutants. Ultrastructural analysis of tom-1 mutants revealed a 50% reduction in presynaptic dense-core vesicles (DCVs) corresponding to enhanced neuropeptide release. Conversely, overexpression of TOM-1 led to an accumulation of DCVs. Together, these data provide the first in vivo evidence that TOM-1 negatively regulates DCV exocytosis. In C. elegans, neuropeptide release is promoted by the calcium-dependent activator protein for secretion (CAPS) homolog UNC-31. To test for a genetic interaction between tomosyn and CAPS, we generated tom-1;unc-31 double mutants. Loss of TOM-1 suppressed the behavioral, electrophysiological, and DCV ultrastructural phenotypes of unc-31 mutants, indicating that TOM-1 antagonizes UNC-31-dependent DCV release. Because unc-31 mutants exhibit synaptic transmission defects, we postulated that loss of DCV release in these mutants and the subsequent suppression by tom-1 mutants could simply reflect alterations in synaptic activity, rather than direct regulation of DCV release. To distinguish between these two possibilities, we analyzed C. elegans Rim mutants (unc-10), which have a comparable reduction in synaptic transmission to unc-31 mutants, specifically attributed to defects in synaptic vesicle (SV) exocytosis. Based on this analysis, we conclude that the changes in DCV release in tom-1 and unc-31 mutants reflect direct effects of TOM-1 and UNC-31 on DCV exocytosis, rather than altered SV release.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCalmodulinDown-RegulationMutationPeptidesPresynaptic TerminalsSecretory VesiclesSynapsesCaenorhabditis elegans ProteinsCalmodulinPeptidestom-1 protein, C elegans

Identifiers

PMID17881523
PMCPMC3874420
OpenAlexW1978244725

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.