Li JiangLi, Xiao Yang, Zhou Wei, Wu ZhengXing, Zhang RongYing, Xu Tao
Key Laboratory of Molecular Biophysics of the Ministry of Education, Institute of Biophysics and Biochemistry, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Sci China C Life Sci. 2009 Dec;52(12):1156-63. doi: 10.1007/s11427-009-0160-y. Epub 2009 Dec 17.
Synaptotagmin VII (Syt VII), which has a higher Ca(2+) affinity and slower disassembly kinetics with lipid than Syt I and Syt IX, was regarded as being uninvolved in synaptic vesicle (SV) exocytosis but instead possibly as a calcium sensor for the slower kinetic phase of dense core vesicles (DCVs) release. By using high temporal resolution capacitance and amperometry measurements, it was demonstrated that the knockdown of endogenous Syt VII attenuated the fusion of DCV with the plasma membrane, reduced the amplitude of the exocytotic burst of the Ca(2+)-triggered DCV release without affecting the slope of the sustained component, and blocked the fusion pore expansion. This suggests that Syt VII is the Ca(2+) sensor of DCV fusion machinery and is an essential factor for the establishment and maintenance of the pool size of releasable DCVs in PC12 cells.
与突触结合蛋白I和突触结合蛋白IX相比，突触结合蛋白VII（Syt VII）对Ca(2+)具有更高的亲和力，与脂质的解离动力学更慢，被认为不参与突触小泡（SV）的胞吐作用，而是可能作为致密核心囊泡（DCV）释放较慢动力学阶段的钙传感器。通过使用高时间分辨率电容和安培测量法，结果表明，内源性Syt VII的敲低减弱了DCV与质膜的融合，降低了Ca(2+)触发的DCV释放的胞吐爆发幅度，而不影响持续成分的斜率，并阻断了融合孔的扩张。这表明Syt VII是DCV融合机制的Ca(2+)传感器，是PC12细胞中可释放DCV池大小建立和维持的关键因素。
