Genetic analysis of Fasciclin II in drosophila: Defasciculation, refasciculation, and altered fasciculation

  • Lin D
  • Fetter R
  • Kopczynski C
 et al. 
  • 61

    Readers

    Mendeley users who have this article in their library.
  • 241

    Citations

    Citations of this article.

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 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.

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Authors

  • David M. Lin

  • Richard D. Fetter

  • Casey Kopczynski

  • Gabriele Grenningloh

  • Corey S. Goodman

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free