ZFIN ID: ZDB-PUB-090319-17
Apc1-Mediated Antagonism of Wnt/beta-Catenin Signaling Is Required for Retino-Tectal Pathfinding in the Zebrafish
Paridaen, J.T., Danesin, C., Elas, A.T., van de Water, S., Houart, C., and Zivkovic, D.
Date: 2009
Source: Zebrafish   6(1): 41-47 (Journal)
Registered Authors: Danesin, Cathy, Houart, Corinne
Keywords: none
MeSH Terms:
  • Animals
  • Axons
  • Embryo, Nonmammalian
  • Mutation
  • Optic Nerve
  • Retina/cytology
  • Retina/embryology*
  • Retina/metabolism
  • Retinal Ganglion Cells/metabolism
  • Signal Transduction*
  • Tectum Mesencephali/cytology
  • Tectum Mesencephali/embryology*
  • Tectum Mesencephali/metabolism
  • Tumor Suppressor Proteins/genetics
  • Tumor Suppressor Proteins/metabolism*
  • Zebrafish/embryology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • beta Catenin/metabolism*
PubMed: 19292673 Full text @ Zebrafish
The tumor suppressor Apc1 is an intracellular antagonist of the Wnt/beta-catenin pathway. We examined the effects of an Apc1 loss-of-function mutation on retino-tectal axon pathfinding in zebrafish. In apc mutants, the retina is disorganized and optic nerves portray pathfinding defects at the optic chiasm and do not project properly to the tectum. Wild-type cells, transplanted into mutant retinae, acquire retinal ganglion cell fate and project axons that cross at the mispositioned optic chiasm and extend to the contralateral tectum, suggesting a function of apc1 in axon pathfinding. These defects are caused mainly by stabilization of beta-catenin. These data demonstrate that Apc1 function is required for correct patterning of the retina and proper retinal ganglion axon projections.