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A High-content Assay for Monitoring AMPA Receptor Trafficking
Published on: January 28, 2019
A presynaptic endosomal trafficking pathway controls synaptic growth signaling
Avital A Rodal1, Aline D Blunk, Yulia Akbergenova
1Department of Biology, The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. arodal@brandeis.edu
The Journal of Cell Biology
|April 6, 2011
Summary
Nervous Wreck (Nwk) and sorting nexin 16 (SNX16) proteins control synaptic growth signaling by regulating endosomal trafficking. This pathway is essential for neuronal function and involves the endosomal sorting complex required for transport (ESCRT) machinery.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Synaptic plasticity involves structural remodeling driven by growth signals, altering neuronal function.
- Endocytic pathways regulate synaptic growth factor receptor signaling, but cargo trafficking mechanisms are unclear.
Purpose of the Study:
- To elucidate the mechanisms controlling cargo traffic between endocytic compartments in presynaptic neurons.
- To define the role of Nervous Wreck (Nwk) and sorting nexin 16 (SNX16) in synaptic growth signaling.
Main Methods:
- Investigated physical interactions between Nwk and SNX16 using Drosophila melanogaster models.
- Utilized live imaging in neurons to track endosomal compartments.
- Identified alternative signal termination pathways involving the endosomal sorting complex required for transport (ESCRT).
Main Results:
- Nwk physically interacts with SNX16, a key regulator of bone morphogenic protein receptor signaling.
- SNX16-positive early endosomes transiently interact with Nwk-containing recycling endosomes.
- An ESCRT-dependent pathway terminates signaling in the absence of SNX16.
Conclusions:
- Defined a presynaptic trafficking pathway involving SNX16, Nwk, and ESCRT.
- This pathway controls synaptic growth signaling at the endosomal compartment interface.
- Identified novel mechanisms for regulating neuronal plasticity and function.
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