μ2 adaptin facilitates but is not essential for synaptic vesicle recycling in Caenorhabditis elegans

Author:

Gu Mingyu1,Schuske Kim1,Watanabe Shigeki1,Liu Qiang1,Baum Paul23,Garriga Gian2,Jorgensen Erik M.1

Affiliation:

1. Howard Hughes Medical Institute and Department of Biology, University of Utah, Salt Lake City, UT 84112

2. Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720

3. Division of Experimental Medicine, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, CA 94110

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 (μ2) 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 μ2 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 μ2 facilitates but is not essential for synaptic vesicle recycling.

Publisher

Rockefeller University Press

Subject

Cell Biology

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