Genetic analysis of Fasciclin II in Drosophila: defasciculation, refasciculation, and altered fasciculation

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / ultrastructure
  • Cell Adhesion Molecules, Neuronal / genetics*
  • Cell Adhesion Molecules, Neuronal / metabolism
  • Central Nervous System / embryology
  • Drosophila melanogaster / embryology
  • Drosophila melanogaster / genetics
  • Female
  • Male
  • Microscopy, Electron
  • Neural Pathways / embryology


  • Cell Adhesion Molecules, Neuronal
  • fasciclin II