FIGURE

Figure 10

ID

ZDB-FIG-200711-11

Publication

Sun et al., 2020 - Fgfr3 mutation disrupts chondrogenesis and bone ossification in zebrafish model mimicking CATSHL syndrome partially via enhanced Wnt/β-catenin signaling

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Figure 10

Schematic diagram of the mechanisms underlying the role of fgfr3 in zebrafish skeleton development. Deletion of Fgfr3 in zebrafish results in enhanced IHH signaling and up-regulated canonical Wnt/β-catenin signaling that may lead to increased chondrocyte proliferation, abnormal hypertrophy and disordered arrangement of chondrocytes in growth plates. Fgfr3 mutation leads to decreased proliferation and differentiation of osteoblasts and decreased mineralization in skull bone. A combination of above mechanisms may lead to disrupted chondrogenesis and bone ossification resulting in craniofacial skeleton malformation in fgfr3 mutant zebrafish.

Expression Data

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