Evidence map›Paper›PMID 24353060›Full record

ArticleDevelopment (Cambridge, England)2014

Postsynaptic glutamate receptors regulate local BMP signaling at the Drosophila neuromuscular junction.

Mikolaj Sulkowski, Young-Jun Kim, Mihaela Serpe

Abstract 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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

  1. The Effects of CaMembranes · 2026
    Article
  2. Article
  3. Article
  4. Journal of biological rhythms · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Postsynaptic BMP signaling regulates myonuclear properties inbioRxiv : the preprint server for biology · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. BMP/TGF-β signaling as a modulator of neurodegeneration in ALS.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    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

3 authors at 1 institution in 1 country.

Mikolaj SulkowskiProgram in Cellular Regulation and Metabolism, NICHD, NIH, Bethesda, MD 20892, USA.
Young-Jun Kim
Mihaela Serpe
Eunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Mechanisms of synapse developmentZIAHD008914 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SERPE, MIHAELA · 2011 to 2025
$16.4M
Modulation of TGF-beta signalingZIAHD008869 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SERPE, MIHAELA · 2009 to 2025
$8.0M
Intramural NIH HHSNICHD NIH HHS Z01 HD008869NICHD NIH HHS Z01 HD008914
6 · The paper itself

Abstract

Effective communication between pre- and postsynaptic compartments is required for proper synapse development and function. At the Drosophila neuromuscular junction (NMJ), a retrograde BMP signal functions to promote synapse growth, stability and homeostasis and coordinates the growth of synaptic structures. Retrograde BMP signaling triggers accumulation of the pathway effector pMad in motoneuron nuclei and at synaptic termini. Nuclear pMad, in conjunction with transcription factors, modulates the expression of target genes and instructs synaptic growth; a role for synaptic pMad remains to be determined. Here, we report that pMad signals are selectively lost at NMJ synapses with reduced postsynaptic sensitivities. Despite this loss of synaptic pMad, nuclear pMad persisted in motoneuron nuclei, and expression of BMP target genes was unaffected, indicating a specific impairment in pMad production/maintenance at synaptic termini. During development, synaptic pMad accumulation followed the arrival and clustering of ionotropic glutamate receptors (iGluRs) at NMJ synapses. Synaptic pMad was lost at NMJ synapses developing at suboptimal levels of iGluRs and Neto, an auxiliary subunit required for functional iGluRs. Genetic manipulations of non-essential iGluR subunits revealed that synaptic pMad signals specifically correlated with the postsynaptic type-A glutamate receptors. Altering type-A receptor activities via protein kinase A (PKA) revealed that synaptic pMad depends on the activity and not the net levels of postsynaptic type-A receptors. Thus, synaptic pMad functions as a local sensor for NMJ synapse activity and has the potential to coordinate synaptic activity with a BMP retrograde signal required for synapse growth and homeostasis.

Indexed as

AnimalsAnimals, Genetically ModifiedBone Morphogenetic ProteinsDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsMembrane ProteinsNeuromuscular JunctionReceptors, GlutamateReceptors, Ionotropic GlutamateSignal TransductionSynapsesSynaptic TransmissionTranscription FactorsBone Morphogenetic ProteinsDNA-Binding ProteinsDrosophila ProteinsMAD protein, DrosophilaMembrane ProteinsNeto protein, DrosophilaReceptors, GlutamateReceptors, Ionotropic GlutamateTranscription FactorsBMP signalingDrosophilaGlutamate receptorGlutamatergic synapsesNeuromuscular junction

Identifiers

PMID24353060
PMCPMC3879819
OpenAlexW2133909481

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.