Evidence map›Paper›PMID 22184197›Full record

ArticleThe Journal of cell biology2011

Reconstituted synaptotagmin I mediates vesicle docking, priming, and fusion.

Zhao Wang, Huisheng Liu, Yiwen Gu, Edwin R Chapman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 104 citations in OpenAlex.

  1. Alternative splicing of synaptotagmin 7 regulates oligomerization and short-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Phospholipids Differentially Regulate CaACS chemical biology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. The juxtamembrane linker of synaptotagmin 1 regulates CabioRxiv : the preprint server for biology · 2023
    Article
  11. Article
  12. Synaptotagmin rings as high-sensitivity regulators of synaptic vesicle docking and fusion.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. Synaptotagmin 1 oligomerization via the juxtamembrane linker regulates spontaneous and evoked neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. α-Synuclein kinetically regulates the nascent fusion pore dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Doc2 Proteins Are Not Required for the Increased Spontaneous Release Rate in Synaptotagmin-1-Deficient Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  19. Article
  20. Article

10 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

4 authors at 2 institutions in 1 country.

Zhao WangDepartment of Neuroscience, Howard Hughes Medical Institute, University of Wisconsin, Madison, WI 53706, USA.
Huisheng Liu
Yiwen Gu
Edwin R Chapman
Howard Hughes Medical Institute · USUniversity of Wisconsin–Madison · US

Funding

Synaptotagmin C2B Domain as a Ca2+ Sensing ModuleR01MH061876 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI Edwin R Chapman · 2002 to 2026
$7.7M
Howard Hughes Medical InstituteNIMH NIH HHS MH61876NIMH NIH HHS R01 MH061876
6 · The paper itself

Abstract

The synaptic vesicle protein synaptotagmin I (syt) promotes exocytosis via its ability to penetrate membranes in response to binding Ca(2+) and through direct interactions with SNARE proteins. However, studies using full-length (FL) membrane-embedded syt in reconstituted fusion assays have yielded conflicting results, including a lack of effect, or even inhibition of fusion, by Ca(2+). In this paper, we show that reconstituted FL syt promoted rapid docking of vesicles (<1 min) followed by a priming step (3-9 min) that was required for subsequent Ca(2+)-triggered fusion between v- and t-SNARE liposomes. Moreover, fusion occurred only when phosphatidylinositol 4,5-bisphosphate was included in the target membrane. This system also recapitulates some of the effects of syt mutations that alter synaptic transmission in neurons. Finally, we demonstrate that the cytoplasmic domain of syt exhibited mixed agonist/antagonist activity during regulated membrane fusion in vitro and in cells. Together, these findings reveal further convergence of reconstituted and cell-based systems.

Indexed as

Membrane FusionAnimalsCalciumCytoplasmMiceMice, KnockoutMutationNeuronsPhosphatidylinositol 4,5-DiphosphatePhosphatidylserinesSNARE ProteinsSynaptic VesiclesSynaptotagmin ITime FactorsCalciumPhosphatidylinositol 4,5-DiphosphatePhosphatidylserinesSNARE ProteinsSynaptotagmin I

Identifiers

PMID22184197
PMCPMC3246889
OpenAlexW2128292852

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.