ZFIN ID: ZDB-PUB-020913-4
Requirement for endoderm and FGF3 in ventral head skeleton formation
David, N.B., Saint-Etienne, L., Tsang, M., Schilling, T.F., and Rosa, F.M.
Date: 2002
Source: Development (Cambridge, England)   129(19): 4457-4468 (Journal)
Registered Authors: David, Nicholas, Rosa, Frederic, Saint-Etienne, Laure, Schilling, Tom, Tsang, Michael
Keywords: Neural crest, Fate, Cartilage, Endoderm, Patterning, casanova
MeSH Terms:
  • Animals
  • Branchial Region/embryology
  • Cartilage, Articular/embryology
  • Cell Differentiation
  • Endoderm
  • Fibroblast Growth Factor 3
  • Fibroblast Growth Factors/metabolism*
  • Head/embryology
  • High Mobility Group Proteins/genetics
  • High Mobility Group Proteins/metabolism
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism
  • Morphogenesis
  • Neural Crest/cytology
  • Proto-Oncogene Proteins/metabolism*
  • SOX Transcription Factors
  • Signal Transduction*
  • Skull/embryology*
  • Transcription Factors/genetics
  • Transcription Factors/metabolism
  • Zebrafish/embryology
  • Zebrafish/metabolism
  • Zebrafish Proteins*
PubMed: 12223404
The vertebrate head skeleton is derived in part from neural crest cells, which physically interact with head ectoderm, mesoderm and endoderm to shape the pharyngeal arches. The cellular and molecular nature of these interactions is poorly understood, and we explore here the function of endoderm in this process. By genetic ablation and reintroduction of endoderm in zebrafish, we show that it is required for the development of chondrogenic neural crest cells, including their identity, survival and differentiation into arch cartilages. Using a genetic interference approach, we further identify Fgf3 as a critical component of endodermal function that allows the development of posterior arch cartilages. Together, our results reveal for the first time that the endoderm provides differential cues along the anteroposterior axis to control ventral head skeleton development and demonstrate that this function is mediated in part by Fgf3.