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 fasll loss-of-function and gain-of-function phenotypes. Loss-of-function fasll 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. © 1994.
CITATION STYLE
Lin, D. M., Fetter, R. D., Kopczynski, C., Grenningloh, G., & Goodman, C. S. (1994). Genetic analysis of Fasciclin II in drosophila: Defasciculation, refasciculation, and altered fasciculation. Neuron, 13(5), 1055–1069. https://doi.org/10.1016/0896-6273(94)90045-0
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