Betz A, Thakur P, Junge H J, Ashery U, Rhee J S, Scheuss V, Rosenmund C, Rettig J, Brose N
Max-Planck-Institut, für experimentelle Medizin, Abteilung Neurogenetik, AG Molekulare Neurobiologie, Hermann-Rein-Str. 3, D-37075, Göttingen, Germany.
Neuron. 2001 Apr;30(1):183-96. doi: 10.1016/s0896-6273(01)00272-0.
Synaptic neurotransmitter release is restricted to active zones, where the processes of synaptic vesicle tethering, priming to fusion competence, and Ca2+-triggered fusion are taking place in a highly coordinated manner. We show that the active zone components Munc13-1, an essential vesicle priming protein, and RIM1, a Rab3 effector with a putative role in vesicle tethering, interact functionally. Disruption of this interaction causes a loss of fusion-competent synaptic vesicles, creating a phenocopy of Munc13-1-deficient neurons. RIM1 binding and vesicle priming are mediated by two distinct structural modules of Munc13-1. The Munc13-1/RIM1 interaction may create a functional link between synaptic vesicle tethering and priming, or it may regulate the priming reaction itself, thereby determining the number of fusion-competent vesicles.
突触神经递质的释放局限于活性区,在活性区,突触小泡的系留、引发至融合能力以及Ca2+触发的融合过程以高度协调的方式发生。我们发现,活性区成分Munc13-1(一种必需的小泡引发蛋白)和RIM1(一种在小泡系留中具有假定作用的Rab3效应器)在功能上相互作用。这种相互作用的破坏会导致具有融合能力的突触小泡丢失,产生与Munc13-1缺陷神经元相似的表型。RIM1结合和小泡引发由Munc13-1的两个不同结构模块介导。Munc13-1/RIM1相互作用可能在突触小泡系留和引发之间建立功能联系,或者它可能调节引发反应本身,从而决定具有融合能力的小泡数量。