Evidence map›Paper›PMID 25255438›Full record

ArticlePloS one2014

Anterograde Activin signaling regulates postsynaptic membrane potential and GluRIIA/B abundance at the Drosophila neuromuscular junction.

Myung-Jun Kim, Michael B O'Connor

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Postsynaptic BMP signaling regulates myonuclear properties inbioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Dysregulation of BMP, Wnt, and Insulin Signaling in Fragile X Syndrome.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Development (Cambridge, England) · 2021
    Article
  12. FOXO Regulates Neuromuscular Junction Homeostasis DuringFrontiers in aging neuroscience · 2020
    Article
  13. Article
  14. Review
  15. TheBiology open · 2018
    Article
  16. TGF-β Family Signaling inCold Spring Harbor perspectives in biology · 2017
    Review
  17. Activin signaling mediates muscle-to-adipose communication in a mitochondria dysfunction-associated obesity model.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Myung-Jun KimDepartment of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.
Michael B O'ConnorDepartment of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.
University of Minnesota · US

Funding

Regulating TGF-beta Signaling in DrosophilaR01GM095746 · NIGMS · UNIVERSITY OF MINNESOTA · PI O'CONNOR, MICHAEL BRENDAN · 2011 to 2014
$1.3M
NIGMS NIH HHS GM95746NIGMS NIH HHS R01 GM095746
6 · The paper itself

Abstract

Members of the TGF-β superfamily play numerous roles in nervous system development and function. In Drosophila, retrograde BMP signaling at the neuromuscular junction (NMJ) is required presynaptically for proper synapse growth and neurotransmitter release. In this study, we analyzed whether the Activin branch of the TGF-β superfamily also contributes to NMJ development and function. We find that elimination of the Activin/TGF-β type I receptor babo, or its downstream signal transducer smox, does not affect presynaptic NMJ growth or evoked excitatory junctional potentials (EJPs), but instead results in a number of postsynaptic defects including depolarized membrane potential, small size and frequency of miniature excitatory junction potentials (mEJPs), and decreased synaptic densities of the glutamate receptors GluRIIA and B. The majority of the defective smox synaptic phenotypes were rescued by muscle-specific expression of a smox transgene. Furthermore, a mutation in actβ, an Activin-like ligand that is strongly expressed in motor neurons, phenocopies babo and smox loss-of-function alleles. Our results demonstrate that anterograde Activin/TGF-β signaling at the Drosophila NMJ is crucial for achieving normal abundance and localization of several important postsynaptic signaling molecules and for regulating postsynaptic membrane physiology. Together with the well-established presynaptic role of the retrograde BMP signaling, our findings indicate that the two branches of the TGF-β superfamily are differentially deployed on each side of the Drosophila NMJ synapse to regulate distinct aspects of its development and function.

Indexed as

Signal TransductionSynaptic PotentialsActivinsAnimalsDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsLigandsMutationNeuromuscular JunctionProtein TransportReceptors, GlutamateSmad Proteins, Receptor-RegulatedTranscription FactorsTransforming Growth Factor betaTumor Suppressor ProteinsActivinsdlg1 protein, DrosophilaDNA-Binding ProteinsDrosophila ProteinsLigandsMAD protein, DrosophilaReceptors, GlutamateSmad Proteins, Receptor-RegulatedSmox protein, DrosophilaTranscription FactorsTransforming Growth Factor betaTumor Suppressor Proteins

Identifiers

PMID25255438
PMCPMC4177838
OpenAlexW2052299608

What OpenQuestion holds

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LicenceCC BY
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.