Park Yongsoo, Seo Jong Bae, Fraind Alicia, Pérez-Lara Angel, Yavuz Halenur, Han Kyungreem, Jung Seung-Ryoung, Kattan Iman, Walla Peter Jomo, Choi MooYoung, Cafiso David S, Koh Duk-Su, Jahn Reinhard
Department of Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Göttingen, Germany.
Department of Physiology and Biophysics, University of Washington, Seattle, Washington, USA.
Nat Struct Mol Biol. 2015 Oct;22(10):815-23. doi: 10.1038/nsmb.3097. Epub 2015 Sep 21.
The Ca(2+) sensor synaptotagmin-1 is thought to trigger membrane fusion by binding to acidic membrane lipids and SNARE proteins. Previous work has shown that binding is mediated by electrostatic interactions that are sensitive to the ionic environment. However, the influence of divalent or polyvalent ions, at physiological concentrations, on synaptotagmin's binding to membranes or SNAREs has not been explored. Here we show that binding of rat synaptotagmin-1 to membranes containing phosphatidylinositol 4,5-bisphosphate (PIP2) is regulated by charge shielding caused by the presence of divalent cations. Surprisingly, polyvalent ions such as ATP and Mg(2+) completely abrogate synaptotagmin-1 binding to SNAREs regardless of the presence of Ca(2+). Altogether, our data indicate that at physiological ion concentrations Ca(2+)-dependent synaptotagmin-1 binding is confined to PIP2-containing membrane patches in the plasma membrane, suggesting that membrane interaction of synaptotagmin-1 rather than SNARE binding triggers exocytosis of vesicles.
钙离子传感器突触结合蛋白-1被认为通过与酸性膜脂和SNARE蛋白结合来触发膜融合。先前的研究表明,这种结合是由对离子环境敏感的静电相互作用介导的。然而,生理浓度下二价或多价离子对突触结合蛋白与膜或SNAREs结合的影响尚未得到研究。在此我们表明,大鼠突触结合蛋白-1与含磷脂酰肌醇4,5-二磷酸(PIP2)的膜的结合受二价阳离子存在所导致的电荷屏蔽调节。令人惊讶的是,无论有无钙离子,诸如ATP和Mg(2+)等多价离子都会完全消除突触结合蛋白-1与SNAREs的结合。总之,我们的数据表明,在生理离子浓度下,钙离子依赖性突触结合蛋白-1的结合局限于质膜中含PIP2的膜片,这表明突触结合蛋白-1的膜相互作用而非与SNAREs的结合触发了囊泡的胞吐作用。