ZFIN ID: ZDB-PUB-131122-12
Fgf receptors Fgfr1a and Fgfr2 control the function of pharyngeal endoderm in late cranial cartilage development
Larbuisson, A., Dalcq, J., Martial, J.A., and Muller, M.
Date: 2013
Source: Differentiation; research in biological diversity 86(4-5): 192-206 (Journal)
Registered Authors: Martial, Joseph A., Muller, Marc
Keywords: zebrafish, fgfr, signaling, cartilage, BMP
MeSH Terms: Animals; Body Patterning/genetics; Cartilage/growth & development*; Cell Differentiation/genetics*; Chondrogenesis (all 14) expand
PubMed: 24176552 Full text @ Differentiation
ABSTRACT

Cranial cartilage derives mainly from cranial neural crest cells and its formation requires fibroblast growth factor (Fgf) signaling for early differentiation and survival of developing chondrocytes as well as patterning of the endodermal pouches.

Here, we investigate the role of Fgf receptors in chondrocyte maturation at later stages, beyond 24 hpf. Using inducible expression of a dominant-negative Fgf receptor, we show that Fgf signaling is required around 30 hpf for correct cartilage formation. The receptor genes fgfr1a and fgr2 are expressed in pharyngeal endodermal pouches after 24 hpf or 26 hpf, respectively. Depletion of any of these two receptors by microinjection of antisense morpholinos results in severe defects in cartilage formation at 4 dpf and a decrease in expression of the late chondrocyte markers barx1 and runx2b. Although endodermal pouches are correctly formed and patterned, receptor knock down leads to decreased expression of runx3, egr1 and sox9b in this tissue, while expression of fsta, coding for a secreted BMP/TgfΒ inhibitor, is clearly increased. Rescue experiments revealed that each Fgfr1a or Fgfr2 receptor is able to compensate for the loss of the other.

Thus, we show that minimal amounts of Fgfr1a or Fgfr2 are required to initiate a regulatory cascade in pharyngeal endoderm reducing expression of fsta, thereby allowing correct BMP signaling to the maturing chondrocytes of the head cartilage.

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