Lin D M, Fetter R D, Kopczynski C, Grenningloh G, Goodman C S
Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.
Neuron. 1994 Nov;13(5):1055-69. doi: 10.1016/0896-6273(94)90045-0.
The Drosophila neural cell adhesion molecule Fasciclin II (Fas II) is expressed dynamically on a subset of embryonic CNS axons, many of which selectively fasciculate in the vMP2, MP1, and FN3 pathways. Here we show complementary fasII loss-of-function and gain-of-function phenotypes. Loss-of-function fasII mutations lead to the complete or partial defasciculation of all three pathways. Gain-of-function conditions, using a specific control element to direct increased levels of Fas II on the axons in these three pathways, rescue the loss-of-function phenotype. Moreover, the gain-of-function can alter fasciculation by abnormally fusing pathways together, in one case apparently by preventing normal defasciculation. These results define an in vivo function for Fas II as a neuronal recognition molecule that controls one mechanism of growth cone guidance-selective axon fasciculation--and genetically separates this function from other aspects of outgrowth and directional guidance.
果蝇神经细胞黏附分子Fasciclin II（Fas II）在胚胎中枢神经系统轴突的一个亚群上动态表达，其中许多轴突在vMP2、MP1和FN3通路中选择性地成束。在这里，我们展示了互补的fasII功能丧失和功能获得表型。功能丧失的fasII突变导致所有三条通路完全或部分解束。功能获得条件下，使用特定的控制元件来指导这三条通路中轴突上Fas II水平的增加，挽救了功能丧失的表型。此外，功能获得可通过异常地将通路融合在一起而改变成束，在一个案例中显然是通过阻止正常的解束。这些结果确定了Fas II作为一种神经元识别分子在体内的功能，该分子控制生长锥导向的一种机制——选择性轴突成束——并在基因上将该功能与生长和定向导向的其他方面区分开来。
