(A) Wildtype ethmoid plate with associated stacking of chondrocytes. (B) Redrawn examples of ethmoid plate defects observed in zebrafish environmental factor exposure studies (Kuchler et al., 2018; Liu et al., 2020) (Methotrexate 100 μM, Dexamethasone 200 μM, retinoic acid 5 nM and hypoxia). A broad phenotypic range of ethmoid plate defects is observed, indicating that development of the ethmoid plate is affected variously by different compounds. Mild phenotypes include a rough edge to the anterior ethmoid plate, and differential cell morphology (round vs. elongated) and chondrocyte stacking is disordered, drawn from Liu et al. (2020) (scale bar 5 μm). At the other end of the spectrum, phenotypes are observed in which ethmoid plate structures are (partially) missing, indicating effects on migration, differentiation and survival CNCCs. Moreover, some factors affect early as well as late craniofacial development, and various effects can occur though differential exposure times during specific sensitivity windows.
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