Evidence map›Paper›PMID 31387992›Full record

ArticleNature communications2019

Synaptotagmin 17 controls neurite outgrowth and synaptic physiology via distinct cellular pathways.

David A Ruhl, Ewa Bomba-Warczak, Emma T Watson, Mazdak M Bradberry, Tabitha A Peterson, Trina Basu, Alyssa Frelka, Chantell S Evans, Joseph S Briguglio, Tamara Basta and 6 more

Abstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Synaptotagmin 4 Supports Spontaneous Axon Sprouting after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Consistent DNA Hypomethylations in Prostate Cancer.International journal of molecular sciences · 2022
    Article
  16. Review
  17. 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

16 authors.

David A RuhlDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
Ewa Bomba-WarczakDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.ORCID http://orcid.org/0000-0002-1744-3516
Emma T WatsonDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
Mazdak M BradberryDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
Tabitha A PetersonDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, 52242, USA.ORCID http://orcid.org/0000-0003-0780-5795
Trina BasuDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
Alyssa FrelkaDepartment of Anesthesiology, University of Wisconsin, Madison, WI, 53706, USA.
Chantell S EvansDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Joseph S BriguglioDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
Tamara BastaDepartment of Molecular, Cellular and Developmental Biology, University of Colorado at Boulder, Boulder, CO, 80309, USA.
Michael H B StowellDepartment of Molecular, Cellular and Developmental Biology, University of Colorado at Boulder, Boulder, CO, 80309, USA.ORCID http://orcid.org/0000-0001-7250-1419
Jeffrey N SavasDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Avtar RoopraDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
Robert A PearceDepartment of Anesthesiology, University of Wisconsin, Madison, WI, 53706, USA.ORCID http://orcid.org/0000-0002-1516-6260
Robert C PiperDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, 52242, USA.ORCID http://orcid.org/0000-0001-9995-5699
Edwin R ChapmanDepartment of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA. chapman@wisc.edu.

Funding

INTEGRATED TRAINING FOR PHYSICIAN-SCIENTISTST32GM008692 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI BURKARD, MARK E · 1998 to 2020
$10.3M
NEUROSCIENCE TRAINING PROGRAMT32GM007507 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HALLORAN, MARY C · 1985 to 2017
$9.3M
Synaptotagmin C2B Domain as a Ca2+ Sensing ModuleR01MH061876 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI Edwin R Chapman · 2002 to 2026
$7.7M
Training Program In Molecular AND Cellular PharmacologyT32GM008688 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI AUDHYA, ANJON · 1998 to 2020
$6.0M
Structure and dynamics of exocytotic fusion poresR35NS097362 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI CHAPMAN, EDWIN R · 2017 to 2024
$4.6M
Anesthetic Suppression of Memory through disinhibitory circuits in HippocampusR01GM118801 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI PEARCE, ROBERT A · 2016 to 2019
$1.9M
NIGMS NIH HHS T32 GM007507
6 · The paper itself

Abstract

The synaptotagmin (syt) proteins have been widely studied for their role in regulating fusion of intracellular vesicles with the plasma membrane. Here we report that syt-17, an unusual isoform of unknown function, plays no role in exocytosis, and instead plays multiple roles in intracellular membrane trafficking. Syt-17 is localized to the Golgi complex in hippocampal neurons, where it coordinates import of vesicles from the endoplasmic reticulum to support neurite outgrowth and facilitate axon regrowth after injury. Further, we discovered a second pool of syt-17 on early endosomes in neurites. Loss of syt-17 disrupts endocytic trafficking, resulting in the accumulation of excess postsynaptic AMPA receptors and defective synaptic plasticity. Two distinct pools of syt-17 thus control two crucial, independent membrane trafficking pathways in neurons. Function of syt-17 appears to be one mechanism by which neurons have specialized their secretory and endosomal systems to support the demands of synaptic communication over sprawling neurite arbors.

Indexed as

Neuronal OutgrowthSynaptic TransmissionAnimalsCells, CulturedEndoplasmic ReticulumEndosomesExocytosisFemaleGolgi ApparatusHippocampusMaleMiceMice, KnockoutNerve Tissue ProteinsNeuritesNeuronal PlasticityNerve Tissue ProteinsSynaptotagminsSyt17 protein, mouse

Identifiers

PMID31387992
PMCPMC6684635

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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.