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Nat Commun. 2019 Aug 6;10(1):3532. doi: 10.1038/s41467-019-11459-4.

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

Author information

1
Department of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA.
2
Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
3
Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, 52242, USA.
4
Department of Anesthesiology, University of Wisconsin, Madison, WI, 53706, USA.
5
Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
6
Department of Molecular, Cellular and Developmental Biology, University of Colorado at Boulder, Boulder, CO, 80309, USA.
7
Department of Neuroscience, University of Wisconsin, Madison, WI, 53706, USA. chapman@wisc.edu.
8
Howard Hughes Medical Institute, Chevy Chase, MD, 20815, USA. chapman@wisc.edu.

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.

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