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FGF signaling specifies pre‐chondrogenic identity in neural crest derived mesenchyme, but initiation of chondrogenesis requires BMP4 signaling
Author(s) -
Kumar Megha,
Ray Poulomi,
Chapman Susan C.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.907.5
Subject(s) - chondrogenesis , mesenchyme , endoderm , microbiology and biotechnology , neural crest , sox9 , biology , fibroblast growth factor , limb bud , anatomy , cellular differentiation , stem cell , genetics , gene expression , embryo , gene , receptor
The chick middle ear bone, columella, derives from neural crest mesenchyme located proximally in the second pharyngeal arch. Subjacent pharyngeal endoderm is hypothesized as the source of the local signals that specify the pre‐chondrogenic identity of this tissue. Sox9 is induced and maintained in pre‐chondrogenic cells during condensation formation and endochondral ossification. We show that pharyngeal endoderm was sufficient, but not necessary for specifying pre‐chondrogenic identity. Many Fgf genes are expressed specifically in the pharyngeal endoderm subjacent to neural crest derived mesenchyme. Our results show that FGF signaling is both sufficient and required for specification of Sox9 expression and specification of pre‐chondrogenic identity. Further, FGF signaling, by itself, is insufficient for the induction of the chondrogenic marker, Col2a1. BMP4 signaling can induce Sox9 expression, but only in combination with FGF signaling induced Col2a1 expression and, thus, chondrogenesis. Given the spatio‐temporal expression patterns of FGFs and BMPs in the pharyngeal arches, we suggest that this may represent a general mechanism of specifying pre‐chondrogenic identity and chondrogenesis. Grant Funding Source : NIH/NIDCD