Sørensen Jakob B, Wiederhold Katrin, Müller Emil M, Milosevic Ira, Nagy Gábor, de Groot Bert L, Grubmüller Helmut, Fasshauer Dirk
Department of Membrane Biophysics, Max-Planck-Institute for Biophysical Chemistry, Göttingen, Germany.
EMBO J. 2006 Mar 8;25(5):955-66. doi: 10.1038/sj.emboj.7601003. Epub 2006 Feb 23.
During exocytosis a four-helical coiled coil is formed between the three SNARE proteins syntaxin, synaptobrevin and SNAP-25, bridging vesicle and plasma membrane. We have investigated the assembly pathway of this complex by interfering with the stability of the hydrophobic interaction layers holding the complex together. Mutations in the C-terminal end affected fusion triggering in vivo and led to two-step unfolding of the SNARE complex in vitro, indicating that the C-terminal end can assemble/disassemble independently. Free energy perturbation calculations showed that assembly of the C-terminal end could liberate substantial amounts of energy that may drive fusion. In contrast, similar N-terminal mutations were without effects on exocytosis, and mutations in the middle of the complex selectively interfered with upstream maturation steps (vesicle priming), but not with fusion triggering. We conclude that the SNARE complex forms in the N- to C-terminal direction, and that a partly assembled intermediate corresponds to the primed vesicle state.
在胞吐作用过程中,Syntaxin、突触囊泡蛋白和SNAP-25这三种SNARE蛋白之间会形成一个四螺旋卷曲螺旋结构,将囊泡和质膜连接起来。我们通过干扰维持该复合物稳定的疏水相互作用层的稳定性,研究了这个复合物的组装途径。C末端的突变影响了体内的融合触发,并导致SNARE复合物在体外分两步展开,这表明C末端可以独立组装/拆卸。自由能微扰计算表明,C末端的组装可以释放大量可能驱动融合的能量。相比之下,类似的N末端突变对胞吐作用没有影响,复合物中间部分的突变则选择性地干扰了上游成熟步骤(囊泡引发),但不影响融合触发。我们得出结论,SNARE复合物是从N末端向C末端方向形成的,并且部分组装的中间体对应于引发的囊泡状态。