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Neuron. 1994 Nov;13(5):1055-69.

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

Author information

1
Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.

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.

PMID:
7946345
DOI:
10.1016/0896-6273(94)90045-0
[Indexed for MEDLINE]

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