Genetic analysis of Fasciclin II in Drosophila: defasciculation, refasciculation, and altered fasciculation.
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.
Lin
D M
DM
Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.
Fetter
R D
RD
Kopczynski
C
C
Grenningloh
G
G
Goodman
C S
CS
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics* / Q000378:metabolism; D002490:Central Nervous System / Q000196:embryology; D004331:Drosophila melanogaster / Q000196:embryology / Q000235:genetics; D005260:Female; D008297:Male; D008854:Microscopy, Electron; D009434:Neural Pathways / Q000196:embryology
D015816:Cell Adhesion Molecules, Neuronal; C051642:fasciclin II