Evidence map›Paper›PMID 25066865›Full record

ArticleMolecular and cellular neurosciences2014

Postsynaptic actin regulates active zone spacing and glutamate receptor apposition at the Drosophila neuromuscular junction.

Aline D Blunk, Yulia Akbergenova, Richard W Cho, Jihye Lee, Uwe Walldorf, Ke Xu, Guisheng Zhong, Xiaowei Zhuang, J Troy Littleton

Abstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Postsynaptic BMP signaling regulates myonuclear properties inbioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Molecular Logic of Synaptic Diversity BetweenbioRxiv : the preprint server for biology · 2023
    Article
  10. Article
  11. Review
  12. GABAergic System Dysfunction in Autism Spectrum Disorders.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. HumanNeural plasticity · 2017
    Article
  18. Article
  19. Shank Modulates Postsynaptic Wnt Signaling to Regulate Synaptic Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    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

9 authors.

Aline D BlunkThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, United States.
Yulia AkbergenovaThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, United States.
Richard W ChoThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, United States.
Jihye LeeThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; The Department of Oral Pathology, School of Dentistry, Pusan National University, Republic of Korea.
Uwe WalldorfDepartment of Developmental Biology, University of Saarland, Homburg, Saar, Germany.
Ke XuHoward Hughes Medical Institute (HHMI), Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, United States.
Guisheng ZhongHoward Hughes Medical Institute (HHMI), Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, United States.
Xiaowei ZhuangHoward Hughes Medical Institute (HHMI), Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, United States; Department of Physics, Harvard University, Cambridge, MA 02138, United States.
J Troy LittletonThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, United States; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, United States. Electronic address: troy@mit.edu.

Funding

CHARACTERIZATION OF THE DROSOPHILA SYNAPTOTAGMIN FAMILYR01NS040296 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LITTLETON, J. TROY · 2000 to 2024
$7.9M
NINDS NIH HHS NS40296NINDS NIH HHS R01 NS040296
6 · The paper itself

Abstract

Synaptic communication requires precise alignment of presynaptic active zones with postsynaptic receptors to enable rapid and efficient neurotransmitter release. How transsynaptic signaling between connected partners organizes this synaptic apparatus is poorly understood. To further define the mechanisms that mediate synapse assembly, we carried out a chemical mutagenesis screen in Drosophila to identify mutants defective in the alignment of active zones with postsynaptic glutamate receptor fields at the larval neuromuscular junction. From this screen we identified a mutation in Actin 57B that disrupted synaptic morphology and presynaptic active zone organization. Actin 57B, one of six actin genes in Drosophila, is expressed within the postsynaptic bodywall musculature. The isolated allele, act(E84K), harbors a point mutation in a highly conserved glutamate residue in subdomain 1 that binds members of the Calponin Homology protein family, including spectrin. Homozygous act(E84K) mutants show impaired alignment and spacing of presynaptic active zones, as well as defects in apposition of active zones to postsynaptic glutamate receptor fields. act(E84K) mutants have disrupted postsynaptic actin networks surrounding presynaptic boutons, with the formation of aberrant actin swirls previously observed following disruption of postsynaptic spectrin. Consistent with a disruption of the postsynaptic actin cytoskeleton, spectrin, adducin and the PSD-95 homolog Discs-Large are all mislocalized in act(E84K) mutants. Genetic interactions between act(E84K) and neurexin mutants suggest that the postsynaptic actin cytoskeleton may function together with the Neurexin-Neuroligin transsynaptic signaling complex to mediate normal synapse development and presynaptic active zone organization.

Indexed as

ActinsAge FactorsAnimalsAnimals, Genetically ModifiedCalcium-Binding ProteinsCalponinsDrosophilaDrosophila ProteinsGene Expression RegulationGlutamic AcidGreen Fluorescent ProteinsHorseradish PeroxidaseLarvaMicrofilament ProteinsMicroscopy, Electron, TransmissionModels, MolecularActinsCalcium-Binding ProteinsCalponinsDrosophila Proteinsglutamate receptor III, DrosophilaGlutamic AcidGreen Fluorescent ProteinsHorseradish PeroxidaseMicrofilament ProteinsNerve Tissue Proteinspostsynaptic density proteinsReceptors, GlutamateActinCytoskeletonNeurexinNMJSpectrinSynapse

Identifiers

PMID25066865
PMCPMC4134997

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Registered trials

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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.