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

Abstract

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.

• Authors: D M Lin, R D Fetter, C Kopczynski, G Grenningloh, C S Goodman
• Journal: Neuron (Neuron) Vol. 13 Issue 5 Pg. 1055-69 (Nov 1994) ISSN: 0896-6273 [Print] United States
• PMID: 7946345 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Cell Adhesion Molecules, Neuronal
• fasciclin II

Topics

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