Journal article
Synaptotagmin 17 controls neurite outgrowth and synaptic physiology via distinct cellular pathways
Nature communications, Vol.10(1), pp.3532-14
08/06/2019
DOI: 10.1038/s41467-019-11459-4
PMCID: PMC6684635
PMID: 31387992
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.
Details
- Title: Subtitle
- Synaptotagmin 17 controls neurite outgrowth and synaptic physiology via distinct cellular pathways
- Creators
- David A Ruhl - University of Wisconsin–MadisonEwa Bomba-Warczak - Northwestern UniversityEmma T Watson - University of Wisconsin–MadisonMazdak M Bradberry - University of Wisconsin–MadisonTabitha A Peterson - University of IowaTrina Basu - University of Wisconsin–MadisonAlyssa Frelka - University of Wisconsin–MadisonChantell S Evans - University of PennsylvaniaJoseph S Briguglio - University of Wisconsin–MadisonTamara Basta - University of Colorado BoulderMichael H B Stowell - University of Colorado BoulderJeffrey N Savas - Northwestern UniversityAvtar Roopra - University of Wisconsin–MadisonRobert A Pearce - University of Wisconsin–MadisonRobert C Piper - University of IowaEdwin R Chapman - University of Wisconsin–Madison
- Resource Type
- Journal article
- Publication Details
- Nature communications, Vol.10(1), pp.3532-14
- DOI
- 10.1038/s41467-019-11459-4
- PMID
- 31387992
- PMCID
- PMC6684635
- NLM abbreviation
- Nat Commun
- ISSN
- 2041-1723
- eISSN
- 2041-1723
- Grant note
- T32 GM007507 / NIGMS NIH HHS R35 NS097362 / NINDS NIH HHS R01 MH061876 / NIMH NIH HHS T32 GM008692 / NIGMS NIH HHS R01 GM118801 / NIGMS NIH HHS T32 GM008688 / NIGMS NIH HHS
- Language
- English
- Date published
- 08/06/2019
- Academic Unit
- Molecular Physiology and Biophysics; Medicine Administration; Internal Medicine
- Record Identifier
- 9984297512202771
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