Evidence map›Paper›PMID 26108535›Full record

ArticleThe EMBO journal2015

Regulation of synaptic activity by snapin-mediated endolysosomal transport and sorting.

Jerome Di Giovanni, Zu-Hang Sheng

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-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

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. BORC assemblies integrate BLOC-1 subunits to diversify endosomal trafficking functions.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Physiological and Pathological Roles of the Cytohesin Family in Neurons.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Snapin Specifically Up-Regulates CaInternational journal of molecular sciences · 2021
    Article
  13. Article
  14. Article
  15. Autophagy and the endolysosomal system in presynaptic function.Cellular and molecular life sciences : CMLS · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Jerome Di GiovanniSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Zu-Hang ShengSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA shengz@ninds.nih.gov.
National Institutes of Health · US

Funding

Regulation of mitochondrial transport and its impact on synaptic transmissionZIANS003029 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$31.5M
Transport and regulation of presynaptic release machineryZIANS002946 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$25.6M
AHRQ HHS ZIA HS003029Intramural NIH HHS ZIA NS002946Intramural NIH HHS ZIA NS003029
6 · The paper itself

Abstract

Recycling synaptic vesicles (SVs) transit through early endosomal sorting stations, which raises a fundamental question: are SVs sorted toward endolysosomal pathways? Here, we used snapin mutants as tools to assess how endolysosomal sorting and trafficking impact presynaptic activity in wild-type and snapin(-/-) neurons. Snapin acts as a dynein adaptor that mediates the retrograde transport of late endosomes (LEs) and interacts with dysbindin, a subunit of the endosomal sorting complex BLOC-1. Expressing dynein-binding defective snapin mutants induced SV accumulation at presynaptic terminals, mimicking the snapin(-/-) phenotype. Conversely, over-expressing snapin reduced SV pool size by enhancing SV trafficking to the endolysosomal pathway. Using a SV-targeted Ca(2+) sensor, we demonstrate that snapin-dysbindin interaction regulates SV positional priming through BLOC-1/AP-3-dependent sorting. Our study reveals a bipartite regulation of presynaptic activity by endolysosomal trafficking and sorting: LE transport regulates SV pool size, and BLOC-1/AP-3-dependent sorting fine-tunes the Ca(2+) sensitivity of SV release. Therefore, our study provides new mechanistic insights into the maintenance and regulation of SV pool size and synchronized SV fusion through snapin-mediated LE trafficking and endosomal sorting.

Indexed as

Models, NeurologicalAnimalsBiological TransportBlotting, WesternCalciumCell FractionationCells, CulturedCircular DichroismDysbindinDystrophin-Associated ProteinsImmunohistochemistryLysosomesMiceMicroscopy, ElectronNeuronsSynaptic TransmissionCalciumDtnbp1 protein, mouseDysbindinDystrophin-Associated ProteinsSnapin protein, mouseVesicular Transport ProteinsBLOC‐1dynein motordysbindinendosomal sorting and transportsnapin

Identifiers

PMID26108535
PMCPMC4551352
OpenAlexW2149537461

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.