Evidence map›Paper›PMID 25359729›Full record

ArticleDevelopment (Cambridge, England)2014

Regulation of synaptic development and function by the Drosophila PDZ protein Dyschronic.

James E C Jepson, Mohammed Shahidullah, Die Liu, Sylvain J le Marchand, Sha Liu, Mark N Wu, Irwin B Levitan, Matthew B Dalva, Kyunghee Koh

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular Logic of Synaptic Diversity BetweenbioRxiv : the preprint server for biology · 2023
    Article
  4. Article
  5. Review
  6. AFrontiers in cell and developmental biology · 2022
    Article
  7. Article
  8. TheGenome research · 2021
    Article
  9. Impaired Pre-Motor Circuit Activity and Movement in a Drosophila Model of KCNMA1-Linked Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

9 authors at 3 institutions in 2 countries.

James E C JepsonDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA UCL Institute of Neurology, London WC1N 3BG, UK.
Mohammed ShahidullahDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Die LiuDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Sylvain J le MarchandDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Sha LiuDepartment of Neurology, John Hopkins University, Baltimore, MD 21287, USA.
Mark N WuDepartment of Neurology, John Hopkins University, Baltimore, MD 21287, USA.
Irwin B LevitanDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Matthew B DalvaDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Kyunghee KohDepartment of Neuroscience, The Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA kyunghee.koh@jefferson.edu.
Thomas Jefferson University · USJefferson Hospital for Neuroscience · USUniversity College London · GB

Funding

Cell-Contact Mediated Mechanisms Assembling Synapses (R01DA022727)R01DA022727 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI DALVA, MATTHEW B · 2007 to 2025
$5.2M
REGULATION OF ION CHANNELS IN NERVE CELLSR01NS017910 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI LEVITAN, IRWIN B · 1985 to 2009
$3.9M
Genetic Analysis of Sleep RegulationR01NS079584 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WU, MARK N · 2012 to 2020
$3.2M
Glial Control of Neuronal Progenitor Cell MigrationR01MH100093 · NIMH · THOMAS JEFFERSON UNIVERSITY · PI DALVA, MATTHEW B · 2013 to 2017
$1.9M
Function of SLEEPLESS in sleep regulationR01GM088221 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI KOH, KYUNGHEE · 2009 to 2013
$1.4M
NIDA NIH HHS DA022727NIDA NIH HHS R01 DA022727NIGMS NIH HHS GM088221NIGMS NIH HHS R01 GM088221NIMH NIH HHS MH08642NIMH NIH HHS MH100093NIMH NIH HHS R01 MH100093NINDS NIH HHS NS079584NINDS NIH HHS NS17910NINDS NIH HHS R01 NS017910NINDS NIH HHS R01 NS079584
6 · The paper itself

Abstract

Synaptic scaffold proteins control the localization of ion channels and receptors, and facilitate molecular associations between signaling components that modulate synaptic transmission and plasticity. Here, we define novel roles for a recently described scaffold protein, Dsychronic (DYSC), at the Drosophila larval neuromuscular junction. DYSC is the Drosophila homolog of whirlin/DFNB31, a PDZ domain protein linked to Usher syndrome, the most common form of human deaf-blindness. We show that DYSC is expressed presynaptically and is often localized adjacent to the active zone, the site of neurotransmitter release. Loss of DYSC results in marked alterations in synaptic morphology and cytoskeletal organization. Moreover, active zones are frequently enlarged and misshapen in dysc mutants. Electrophysiological analyses further demonstrate that dysc mutants exhibit substantial increases in both evoked and spontaneous synaptic transmission. We have previously shown that DYSC binds to and regulates the expression of the Slowpoke (SLO) BK potassium channel. Consistent with this, slo mutant larvae exhibit similar alterations in synapse morphology, active zone size and neurotransmission, and simultaneous loss of dysc and slo does not enhance these phenotypes, suggesting that dysc and slo act in a common genetic pathway to modulate synaptic development and output. Our data expand our understanding of the neuronal functions of DYSC and uncover non-canonical roles for the SLO potassium channel at Drosophila synapses.

Indexed as

AnimalsDrosophilaDrosophila ProteinsImmunohistochemistryLarge-Conductance Calcium-Activated Potassium ChannelsLarvaMembrane PotentialsMembrane ProteinsMicroscopy, ConfocalNeuromuscular JunctionPatch-Clamp TechniquesPDZ DomainsReverse Transcriptase Polymerase Chain ReactionSynapsesDrosophila ProteinsDYSC protein, DrosophilaLarge-Conductance Calcium-Activated Potassium ChannelsMembrane Proteinsslo protein, DrosophilaActive zoneBK channelDrosophilaNeuromuscular junctionPDZ domainScaffold protein

Identifiers

PMID25359729
PMCPMC4302934
OpenAlexW2036958096

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.