Evidence map›Paper›PMID 39719826›Full record

ArticleBiophysical journal2025

Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1.

Maria Tsemperouli, Sudheer Kumar Cheppali, Félix Rivera-Molina, David Chetrit, Ane Landajuela, Derek Toomre, Erdem Karatekin

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biophysical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Membrane fusion and budding.Biophysical journal · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Maria TsemperouliCellular and Molecular Physiology, School of Medicine, Yale University, New Haven, Connecticut; Nanobiology Institute, Yale University, West Haven, Connecticut.
Sudheer Kumar CheppaliCellular and Molecular Physiology, School of Medicine, Yale University, New Haven, Connecticut; Nanobiology Institute, Yale University, West Haven, Connecticut.
Félix Rivera-MolinaCell Biology, School of Medicine, Yale University, New Haven, Connecticut; CINEMA Lab, School of Medicine, Yale University, New Haven, Connecticut.
David ChetritCellular and Molecular Physiology, School of Medicine, Yale University, New Haven, Connecticut; Nanobiology Institute, Yale University, West Haven, Connecticut.
Ane LandajuelaCellular and Molecular Physiology, School of Medicine, Yale University, New Haven, Connecticut; Nanobiology Institute, Yale University, West Haven, Connecticut.
Derek ToomreCell Biology, School of Medicine, Yale University, New Haven, Connecticut; CINEMA Lab, School of Medicine, Yale University, New Haven, Connecticut.
Erdem KaratekinCellular and Molecular Physiology, School of Medicine, Yale University, New Haven, Connecticut; Nanobiology Institute, Yale University, West Haven, Connecticut; Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut; Saints-Pères Paris Institute for the Neurosciences (SPPIN), Université de Paris, Centre National de la Recherche Scientifique (CNRS) UMR 8003, Paris, France; Wu Tsai Institute, Yale University, New Haven, Connecticut. Electronic address: erdem.karatekin@yale.edu.

Funding

Dynamics of membrane tension and synaptic vesicle recyclingR01NS122388 · NINDS · YALE UNIVERSITY · PI KARATEKIN, ERDEM, MACHTA, BENJAMIN BROOKS · 2021 to 2025
$2.2M
Nucleation and dynamics of exocytotic fusion poresR01NS113236 · NINDS · YALE UNIVERSITY · PI KARATEKIN, ERDEM · 2019 to 2023
$1.8M
NINDS NIH HHS R01 NS113236NINDS NIH HHS R01 NS122388
6 · The paper itself

Abstract

Synaptotagmin-1 (Syt1) is a major calcium sensor for rapid neurotransmitter release in neurons and hormone release in many neuroendocrine cells. It possesses two tandem cytosolic C2 domains that bind calcium, negatively charged phospholipids, and the neuronal SNARE complex. Calcium binding to Syt1 triggers exocytosis, but how this occurs is not well understood. Syt1 has additional roles in docking dense-core vesicles (DCVs) and synaptic vesicles to the plasma membrane and in regulating fusion pore dynamics. Thus, Syt1 perturbations could affect release through vesicle docking, fusion triggering, fusion pore regulation, or a combination of these. Here, using a human neuroendocrine cell line, we show that neutralization of highly conserved polybasic patches in either C2 domain of Syt1 impairs both DCV docking and efficient release of serotonin from DCVs. Interestingly, the same mutations resulted in larger fusion pores and faster release of serotonin during individual fusion events. Thus, Syt1's roles in vesicle docking, fusion triggering, and fusion pore control may be functionally related.

Indexed as

CalciumMembrane FusionNeuronsSecretory VesiclesSynaptotagmin ICell LineHumansMutationSerotoninCalciumSerotoninSynaptotagmin I

Identifiers

PMID39719826
PMCPMC12256845

What Socratic 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 Socratic graph.