Evidence map›Paper›PMID 24198381›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Retrograde BMP signaling at the synapse: a permissive signal for synapse maturation and activity-dependent plasticity.

Brett Berke, Jessica Wittnam, Elizabeth McNeill, David L Van Vactor, Haig Keshishian

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

77 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  3. Journal of biological rhythms · 2025
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  10. Identification of secretory autophagy as a mechanism modulating activity-induced synaptic remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Review
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  19. BMP/TGF-β signaling as a modulator of neurodegeneration in ALS.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Article
  20. Article

17 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Brett BerkeMolecular, Cellular, and Developmental Biology Department, Yale University, New Haven, Connecticut 06520, and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115.
Jessica Wittnam
Elizabeth McNeill
David L Van Vactor
Haig Keshishian
Harvard University · USYale University · US

Funding

Smn Regulation of Neuromuscular Morphogenesis in DrosophilaP01NS066888 · NINDS · HARVARD MEDICAL SCHOOL · PI ARTAVANIS-TSAKONAS, SPYRIDON · 2010 to 2014
$6.7M
CELLULAR AND MOLECULAR MECHANISMS OF SYNAPTOGENESISR01NS031651 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 1993 to 2013
$4.2M
Novel Molecular Tools for Transsynaptic Circuit AnalysisR21NS053807 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 2006 to 2007
$352k
Modulation of Inhibitory Synapses by HIV-1 Proteins and CannabinoidsF32DA034997 · NIDA · UNIVERSITY OF MINNESOTA · PI HARGUS, NICHOLAS · 2013 to 2014
$75k
NIDA NIH HHS F32DA034997NINDS NIH HHS 1R21NS053807NINDS NIH HHS P01 NS066888NINDS NIH HHS R01 NS031651NINDS NIH HHS R21 NS053807
6 · The paper itself

Abstract

At the Drosophila neuromuscular junction (NMJ), the loss of retrograde, trans-synaptic BMP signaling causes motoneuron terminals to have fewer synaptic boutons, whereas increased neuronal activity results in a larger synapse with more boutons. Here, we show that an early and transient BMP signal is necessary and sufficient for NMJ growth as well as for activity-dependent synaptic plasticity. This early critical period was revealed by the temporally controlled suppression of Mad, the SMAD1 transcriptional regulator. Similar results were found by genetic rescue tests involving the BMP4/5/6 ligand Glass bottom boat (Gbb) in muscle, and alternatively the type II BMP receptor Wishful Thinking (Wit) in the motoneuron. These observations support a model where the muscle signals back to the innervating motoneuron's nucleus to activate presynaptic programs necessary for synaptic growth and activity-dependent plasticity. Molecular genetic gain- and loss-of-function studies show that genes involved in NMJ growth and plasticity, including the adenylyl cyclase Rutabaga, the Ig-CAM Fasciclin II, the transcription factor AP-1 (Fos/Jun), and the adhesion protein Neurexin, all depend critically on the canonical BMP pathway for their effects. By contrast, elevated expression of Lar, a receptor protein tyrosine phosphatase found to be necessary for activity-dependent plasticity, rescued the phenotypes associated with the loss of Mad signaling. We also find that synaptic structure and function develop using genetically separable, BMP-dependent mechanisms. Although synaptic growth depended on Lar and the early, transient BMP signal, the maturation of neurotransmitter release was independent of Lar and required later, ongoing BMP signaling.

Indexed as

Adenylyl CyclasesAnimalsAnimals, Genetically ModifiedBone Morphogenetic ProteinsCell Adhesion Molecules, NeuronalDrosophilaDrosophila ProteinsGene Expression Regulation, DevelopmentalMotor NeuronsNeuromuscular JunctionNeuronal PlasticityNeuronsReceptor-Like Protein Tyrosine PhosphatasesReceptors, Cell SurfaceSignal TransductionSynapsesAdenylyl CyclasesBone Morphogenetic ProteinsCell Adhesion Molecules, NeuronalDrosophila Proteinsgbb protein, DrosophilaLar protein, DrosophilaNrx protein, DrosophilaReceptor-Like Protein Tyrosine PhosphatasesReceptors, Cell SurfaceRut protein, DrosophilaTransforming Growth Factor betawit protein, Drosophila

Identifiers

PMID24198381
PMCPMC3818560
OpenAlexW2113752547

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.