Fukuda M, Mikoshiba K
Laboratory for Developmental Neurobiology, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, 351-0198, Saitama, Japan.
Neurosci Lett. 2000 Dec 1;295(1-2):33-6. doi: 10.1016/s0304-3940(00)01585-8.
Synaptotagmin I (Syt I), a possible Ca(2+) sensor for neurotransmitter release, was suggested to be involved in neurite outgrowth of chick dorsal root ganglion (DRG) neurons, based on introduction of the antibody against the C2A domain into cells via mechanical lesions. Recently, however, the functional block antibody against the C2A domain was shown to block axonal repair processes, which raised a question as to whether Syt I is indeed involved in neurite outgrowth. In this study, we expressed Syt I or II in PC12 cells and found that these expression did indeed promote neurite outgrowth, as compared to control cells. We further showed that expression of the phospholipid binding activity-deficient mutant of Syt II (Delta180-183) had little effect on the neurite outgrowth of PC12 cells. These results indicate the Ca(2+)/phospholipid binding site of Syt I or II to be essential for neurite outgrowth.
突触结合蛋白I(Syt I)是一种可能参与神经递质释放的钙离子传感器,基于通过机械损伤将针对C2A结构域的抗体引入细胞,有人提出它参与鸡背根神经节(DRG)神经元的轴突生长。然而,最近针对C2A结构域的功能阻断抗体被证明会阻断轴突修复过程,这就引发了一个问题,即Syt I是否真的参与轴突生长。在本研究中,我们在PC12细胞中表达了Syt I或Syt II,发现与对照细胞相比,这些表达确实促进了轴突生长。我们进一步表明,Syt II的磷脂结合活性缺陷突变体(Delta180 - 183)的表达对PC12细胞的轴突生长几乎没有影响。这些结果表明,Syt I或Syt II的钙离子/磷脂结合位点对轴突生长至关重要。