Gu Mingyu, Schuske Kim, Watanabe Shigeki, Liu Qiang, Baum Paul, Garriga Gian, Jorgensen Erik M
Howard Hughes Medical Institute and Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.
J Cell Biol. 2008 Dec 1;183(5):881-92. doi: 10.1083/jcb.200806088.
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.
突触小泡必须循环利用以维持神经传递，这在很大程度上是通过网格蛋白介导的内吞作用实现的。网格蛋白由AP2衔接复合体招募至质膜上的内吞位点。AP2的中间亚基（μ2）与货物蛋白以及细胞表面的磷脂酰肌醇-4,5-二磷酸结合。在此，我们对apm-2基因（也称为dpy-23）进行了表征，该基因编码线虫秀丽隐杆线虫中唯一的μ2亚基。APM-2在神经系统中高度表达并定位于突触；然而神经元中APM-2的特异性缺失并不影响运动。在apm-2突变体中，网格蛋白在突触处定位错误，并且突触小泡数量和诱发反应分别减少至60%和65%。总体而言，这些数据表明AP2的μ2亚基对突触小泡循环利用有促进作用，但并非必不可少。
