header logo image header logo text
Downloads Login
Research
General Information
ZIRC
ZFIN ID: ZDB-PUB-030806-5
Unique and combinatorial functions of Fgf3 and Fgf8 during zebrafish forebrain development
Walshe, J. and Mason, I.
Date: 2003
Source: Development (Cambridge, England) 130(18): 4337-4349 (Journal)
Registered Authors: Mason, Ivor, Walshe, Jenny
Keywords: none
MeSH Terms:
  • Animals
  • Axons/physiology
  • Biomarkers
  • Body Patterning
  • Cell Death
  • Cell Differentiation
  • Cell Division
  • Fibroblast Growth Factor 3
  • Fibroblast Growth Factor 8
  • Fibroblast Growth Factors/genetics
  • Fibroblast Growth Factors/metabolism*
  • Gene Expression Regulation, Developmental*
  • In Situ Hybridization
  • Morphogenesis
  • Oligonucleotides, Antisense/metabolism
  • Prosencephalon/embryology*
  • Prosencephalon/growth & development
  • Prosencephalon/physiology
  • Proto-Oncogene Proteins/genetics
  • Proto-Oncogene Proteins/metabolism*
  • Receptors, Fibroblast Growth Factor/metabolism
  • Signal Transduction/physiology
  • Zebrafish/embryology*
  • Zebrafish Proteins*
PubMed: 12900450 Full text @ Development
ABSTRACT
Complex spatiotemporal expression patterns of fgf3 and fgf8 within the developing zebrafish forebrain suggest their involvement in its regionalisation and early development. These factors have unique and combinatorial roles during development of more posterior brain regions, and here we report similar findings for the developing forebrain. We show that Fgf8 and Fgf3 regulate different aspects of telencephalic development, and that Fgf3 alone is required for the expression of several telencephalic markers. Within the diencephalon, Fgf3 and Fgf8 act synergistically to pattern the ventral thalamus, and are implicated in the regulation of optic stalk formation, whereas loss of Fgf3 alone results in defects in ZLI development. Forebrain commissure formation was abnormal in the absence of either Fgf3 or Fgf8; however, most severe defects were observed in the absence of both. Defects were observed in patterning of both the midline territory, within which the commissures normally form, and neuronal populations, whose axons comprise the commissures. Analysis of embryos treated with an FGFR inhibitor suggests that continuous FGF signalling is required from gastrulation stages for normal forebrain patterning, and identifies additional requirements for FGFR activity.
ADDITIONAL INFORMATION