Evidence map›Paper›PMID 17901219›Full record

ArticleGenes & development2007

Presynaptic establishment of the synaptic cleft extracellular matrix is required for post-synaptic differentiation.

Jeffrey Rohrbough, Emma Rushton, Elvin Woodruff, Tim Fergestad, Krishanthan Vigneswaran, Kendal Broadie

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Activity-Induced Synaptic Structural Modifications by an Activator of Integrin Signaling at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  8. Article
  9. Article
  10. The Matrix Proteins Hasp and Hig Exhibit Segregated Distribution within Synaptic Clefts and Play Distinct Roles in Synaptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Two protein N-acetylgalactosaminyl transferases regulate synaptic plasticity by activity-dependent regulation of integrin signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  17. Article
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  19. 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

6 authors at 1 institution in 1 country.

Jeffrey RohrboughDepartment of Biological Sciences, Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee 37235, USA.
Emma Rushton
Elvin Woodruff
Tim Fergestad
Krishanthan Vigneswaran
Kendal Broadie
John F. Kennedy Center for the Performing Arts · US

Funding

GENETIC ANALYSIS OF SYNAPSE FORMATION AND FUNCTIONR01GM054544 · NIGMS · VANDERBILT UNIVERSITY · PI BROADIE, KENDAL · 1997 to 2010
$2.9M
NIGMS NIH HHS GM54544NIGMS NIH HHS R01 GM054544
6 · The paper itself

Abstract

Formation and regulation of excitatory glutamatergic synapses is essential for shaping neural circuits throughout development. In a Drosophila genetic screen for synaptogenesis mutants, we identified mind the gap (mtg), which encodes a secreted, extracellular N-glycosaminoglycan-binding protein. MTG is expressed neuronally and detected in the synaptic cleft, and is required to form the specialized transsynaptic matrix that links the presynaptic active zone with the post-synaptic glutamate receptor (GluR) domain. Null mtg embryonic mutant synapses exhibit greatly reduced GluR function, and a corresponding loss of localized GluR domains. All known post-synaptic signaling/scaffold proteins functioning upstream of GluR localization are also grossly reduced or mislocalized in mtg mutants, including the dPix-dPak-Dock cascade and the Dlg/PSD-95 scaffold. Ubiquitous or neuronally targeted mtg RNA interference (RNAi) similarly reduce post-synaptic assembly, whereas post-synaptically targeted RNAi has no effect, indicating that presynaptic MTG induces and maintains the post-synaptic pathways driving GluR domain formation. These findings suggest that MTG is secreted from the presynaptic terminal to shape the extracellular synaptic cleft domain, and that the cleft domain functions to mediate transsynaptic signals required for post-synaptic development.

Indexed as

Amino Acid SequenceAnimalsBase SequenceCarrier ProteinsChromosome MappingDNA PrimersDrosophilaDrosophila ProteinsExtracellular MatrixGenes, InsectGlycosaminoglycansMicroscopy, Electron, TransmissionMolecular Sequence DataMutationNeuromuscular JunctionReceptors, GlutamateCarrier ProteinsDNA PrimersDrosophila ProteinsGlycosaminoglycansReceptors, Glutamate

Identifiers

PMID17901219
PMCPMC2000325
OpenAlexW2116552694

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.