Evidence map›Paper›PMID 20554858›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Synaptic homeostasis is consolidated by the cell fate gene gooseberry, a Drosophila pax3/7 homolog.

Bruno Marie, Edward Pym, Sharon Bergquist, Graeme W Davis

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  5. Article
  6. Changes in Presynaptic Gene Expression during Homeostatic Compensation at a Central Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  7. Review
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  12. Cortactin Is a Regulator of Activity-Dependent Synaptic Plasticity Controlled by Wingless.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. Article
  14. Review
  15. Article
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  18. Article
  19. Review
  20. Glial wingless/Wnt regulates glutamate receptor clustering and synaptic physiology at the Drosophila neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
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 1 institution in 1 country.

Bruno MarieDepartment of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California 94158-2822, USA.
Edward Pym
Sharon Bergquist
Graeme W Davis
University of California, San Francisco · US

Funding

SUPPLEMENT FOR RENOVATION OF ANIMAL FACILITIES AT INSTITUTE OF NEUROBIOLOGYG12RR003051 · NCRR · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI FERNANDEZ-REPOLLET, EMMA · 1986 to 2011
$28.1M
TRANSLATIONAL PROTEOMICS CENTERG12MD007600 · NIMHD · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI FERNANDEZ-REPOLLET, EMMA · 2012 to 2016
$11.0M
GENETIC ANALYSIS OF SYNAPTIC HOMEOSTASISR01NS039313 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAVIS, GRAEME W · 2000 to 2016
$5.3M
NCRR NIH HHS G12 RR003051NCRR NIH HHS G12 RR03051NIMHD NIH HHS G12 MD007600NINDS NIH HHS NS39313NINDS NIH HHS R01 NS039313
6 · The paper itself

Abstract

In a large-scale screening effort, we identified the gene gooseberry (gsb) as being necessary for synaptic homeostasis at the Drosophila neuromuscular junction. The gsb gene encodes a pair-rule transcription factor that participates in embryonic neuronal cell fate specification. Here, we define a new postembryonic role for gooseberry. We show that gsb becomes widely expressed in the postembryonic CNS, including within mature motoneurons. Loss of gsb does not alter neuromuscular growth, morphology, or the distribution of essential synaptic proteins. However, gsb function is required postembryonically for the sustained expression of synaptic homeostasis. In GluRIIA mutant animals, miniature EPSP (mEPSP) amplitudes are significantly decreased, and there is a compensatory homeostatic increase in presynaptic release that restores normal muscle excitation. Loss of gsb significantly impairs the homeostatic increase in presynaptic release in the GluRIIA mutant. Interestingly, gsb is not required for the rapid induction of synaptic homeostasis. Furthermore, gsb seems to be specifically involved in the mechanisms responsible for a homeostatic increase in presynaptic release, since it is not required for the homeostatic decrease in presynaptic release observed following an increase in mEPSP amplitude. Finally, Gsb has been shown to antagonize Wingless signaling during embryonic fate specification, and we present initial evidence that this activity is conserved during synaptic homeostasis. Thus, we have identified a gene (gsb) that distinguishes between rapid induction versus sustained expression of synaptic homeostasis and distinguishes between the mechanisms responsible for homeostatic increase versus decrease in synaptic vesicle release.

Indexed as

Animalsbeta-GalactosidaseDrosophilaDrosophila ProteinsDynaminsElectric StimulationEmbryo, NonmammalianExcitatory Postsynaptic PotentialsGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsHomeostasisModels, BiologicalMotor NeuronsMutationNeuromuscular JunctionPatch-Clamp Techniquesbeta-GalactosidaseBRP protein, Drosophiladlg1 protein, DrosophilaDrosophila ProteinsDynaminsglutamate receptor ionotropic, AMPA 2Green Fluorescent ProteinsReceptors, AMPASynapsinsTumor Suppressor Proteins

Identifiers

PMID20554858
PMCPMC3291498
OpenAlexW1993854848

What OpenQuestion holds

Textmetadata
LicenceTDM
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.