Aberle Hermann, Haghighi A Pejmun, Fetter Richard D, McCabe Brian D, Magalhães Tiago R, Goodman Corey S
Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
Neuron. 2002 Feb 14;33(4):545-58. doi: 10.1016/s0896-6273(02)00589-5.
We conducted a large-scale screen for Drosophila mutants that have structural abnormalities of the larval neuromuscular junction (NMJ). We recovered mutations in wishful thinking (wit), a gene that positively regulates synaptic growth. wit encodes a BMP type II receptor. In wit mutant larvae, the size of the NMJs is greatly reduced relative to the size of the muscles. wit NMJs have reduced evoked excitatory junctional potentials, decreased levels of the synaptic cell adhesion molecule Fasciclin II, and synaptic membrane detachment at active zones. Wit is expressed by a subset of neurons, including motoneurons. The NMJ phenotype is specifically rescued by transgenic expression of Wit only in motoneurons. Thus, Wit appears to function as a presynaptic receptor that regulates synaptic size at the Drosophila NMJ.
我们对果蝇幼虫神经肌肉接头(NMJ)存在结构异常的突变体进行了大规模筛选。我们发现了“如意算盘”(wit)基因的突变,该基因正向调控突触生长。wit编码一种BMP II型受体。在wit突变体幼虫中,相对于肌肉大小,NMJ的尺寸大幅减小。wit突变体的NMJ诱发兴奋性突触后电位降低,突触细胞粘附分子Fasciclin II水平下降,且活性区出现突触膜脱离现象。Wit由包括运动神经元在内的一部分神经元表达。仅在运动神经元中通过转基因表达Wit可特异性挽救NMJ表型。因此,Wit似乎作为一种突触前受体发挥作用,调节果蝇NMJ的突触大小。