Shen Kang, Fetter Richard D, Bargmann Cornelia I
Howard Hughes Medical Institute, Department of Anatomy, The University of California, San Francisco, San Francisco, CA 94143, USA.
Cell. 2004 Mar 19;116(6):869-81. doi: 10.1016/s0092-8674(04)00251-x.
Synaptic connections in the nervous system are directed onto specific cellular and subcellular targets. Synaptic guidepost cells in the C. elegans vulval epithelium drive synapses from the HSNL motor neuron onto adjacent target neurons and muscles. Here, we show that the transmembrane immunoglobulin superfamily protein SYG-2 is a central component of the synaptic guidepost signal. SYG-2 is expressed transiently by primary vulval epithelial cells during synapse formation. SYG-2 binds SYG-1, the receptor on HSNL, and directs SYG-1 accumulation and synapse formation to adjacent regions of HSNL. syg-1 and syg-2 mutants have defects in synaptic specificity; the HSNL neuron forms fewer synapses onto its normal targets and forms ectopic synapses onto inappropriate targets. Misexpression of SYG-2 in secondary epithelial cells causes aberrant accumulation of SYG-1 and synaptic markers in HSNL adjacent to the SYG-2-expressing cells. Our results indicate that local interactions between immunoglobulin superfamily proteins can determine specificity during synapse formation.
神经系统中的突触连接指向特定的细胞和亚细胞靶点。秀丽隐杆线虫外阴上皮中的突触导向细胞驱动HSNL运动神经元与相邻的靶神经元和肌肉形成突触。在此，我们表明跨膜免疫球蛋白超家族蛋白SYG-2是突触导向信号的核心成分。SYG-2在突触形成过程中由初级外阴上皮细胞短暂表达。SYG-2与HSNL上的受体SYG-1结合，并将SYG-1的积累和突触形成引导至HSNL的相邻区域。syg-1和syg-2突变体在突触特异性方面存在缺陷；HSNL神经元在其正常靶点上形成的突触较少，并在不适当的靶点上形成异位突触。SYG-2在次级上皮细胞中的错误表达导致SYG-1和突触标记物在与表达SYG-2的细胞相邻的HSNL中异常积累。我们的结果表明，免疫球蛋白超家族蛋白之间的局部相互作用可以在突触形成过程中决定特异性。
