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Updated: Jun 27, 2026

Immobilization of Caenorhabditis elegans to Analyze Intracellular Transport in Neurons
Published on: October 18, 2017
Mu2 adaptin facilitates but is not essential for synaptic vesicle recycling in Caenorhabditis elegans
Mingyu Gu1, Kim Schuske, Shigeki Watanabe
1Howard Hughes Medical Institute and Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.
Abstract:
Synaptic vesicles must be recycled to sustain neurotransmission, in large part via clathrin-mediated endocytosis. Clathrin is recruited to endocytic sites on the plasma membrane by the AP2 adaptor complex. The medium subunit (micro2) of AP2 binds to cargo proteins and phosphatidylinositol-4 ,5-bisphosphate on the cell surface. Here, we characterize the apm-2 gene (also called dpy-23), which encodes the only micro2 subunit in the nematode Caenorhabditis elegans. APM-2 is highly expressed in the nervous system and is localized to synapses; yet specific loss of APM-2 in neurons does not affect locomotion. In apm-2 mutants, clathrin is mislocalized at synapses, and synaptic vesicle numbers and evoked responses are reduced to 60 and 65%, respectively. Collectively, these data suggest AP2 micro2 facilitates but is not essential for synaptic vesicle recycling.
Insights
The AP2 micro2 subunit facilitates synaptic vesicle recycling, crucial for neurotransmission. Loss of this protein impairs clathrin function at synapses but is not essential for vesicle recycling.
Area of Science:
- Neuroscience
- Cell Biology
- Genetics
Background:
- Synaptic vesicle recycling is vital for sustained neurotransmission.
- Clathrin-mediated endocytosis, regulated by the AP2 complex, is a key recycling pathway.
- The AP2 complex's medium subunit (micro2) links cargo and membrane lipids.
Purpose of the Study:
- To characterize the apm-2 gene, encoding the sole micro2 subunit in C. elegans.
- To investigate the role of APM-2 in synaptic vesicle recycling and neurotransmission.
Main Methods:
- Gene characterization of apm-2 in Caenorhabditis elegans.
- Analysis of APM-2 expression and localization in neurons.
- Assessment of synaptic vesicle recycling, clathrin localization, and evoked responses in apm-2 mutants.
Main Results:
- APM-2 is highly expressed in the nervous system and localized to synapses.
- Loss of APM-2 in neurons did not affect locomotion.
- apm-2 mutants exhibited mislocalized clathrin at synapses, reduced synaptic vesicle numbers (60%), and diminished evoked responses (65%).
Conclusions:
- AP2 micro2 facilitates synaptic vesicle recycling.
- AP2 micro2 is not essential for synaptic vesicle recycling.
- AP2 micro2 plays a role in proper clathrin function at synaptic sites.
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