R-Cadherin Is a Pax6-Regulated, Growth-Promoting Cue for Pioneer Axons

• Published in: The Journal of neuroscience Vol. 23; no. 30; pp. 9873 - 9880
• Main Authors: Andrews, Gracie L, Mastick, Grant S
• Format: Journal Article
• Language: English
• Published: United States Soc Neuroscience 29.10.2003; Society for Neuroscience
• Subjects: Animals; Axons - drug effects; Axons - physiology; Cadherins - genetics; Cadherins - metabolism; Cadherins - pharmacology; Cues; Development/Plasticity/Repair; Eye Proteins; Gestational Age; Homeodomain Proteins - metabolism; Homozygote; Mice; Mice, Mutant Strains; Neural Pathways - embryology; Neural Pathways - physiology; Neurons - cytology; Neurons - drug effects; Neurons - metabolism; Paired Box Transcription Factors; PAX6 Transcription Factor; Prosencephalon - cytology; Prosencephalon - embryology; Prosencephalon - metabolism; Repressor Proteins
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/jneurosci.23-30-09873.2003

The transcription factor Pax6 has been implicated in two processes that may be related in brain development: establishment of regional cell adhesion properties and axon guidance. In Pax6 mutant mouse embryos, forebrain pioneer axons make pathfinding errors. These errors occur in a region of the ventral thalamus in which the expression of the cell adhesion molecule R-cadherin (Cdh4) is lost in Pax6 mutants. In vitro, an R-cadherin substrate promoted pioneer axon outgrowth. Furthermore, pioneer axon outgrowth was rescued in vivo by selective replacement of R-cadherin by electroporation into cultured Pax6 mutant embryos. Thus, these studies implicate Pax6 as an early brain patterning gene that establishes regional adhesive codes to guide pioneer axons.