Ethanol induces craniofacial defects in Bmp mutants independent of

Background: Fetal Alcohol Spectrum Disorders (FASD) describes a wide range of neurological defects and craniofacial malformations associated with prenatal ethanol exposure. While there is growing evidence for a genetic component to FASD, little is known of the cellular mechanisms underlying these ethanol-sensitive loci in facial development. Endoderm morphogenesis to form lateral protrusions called pouches is one key mechanism in facial development. We have previously shown that multiple members of the Bone Morphogenetic Pathway (Bmp) signaling pathway, a key regulator of pouch formation, interacts with ethanol disrupting facial development. However, ethanol does not directly impact Bmp signaling suggesting that downstream effectors, like Methods: Here we use an ethanol exposure paradigm with Results: We show that Bmp-ethanol interactions alter morphology of the endodermal pouches, independent of Conclusions: Collectively, our results suggest that ethanol's mode of action is independent of downstream Bmp effectors, converging on CNCC cell survival. Ultimately, our work provides a mechanistic paradigm of ethanol-induced facial defects and connects ethanol exposure with concrete cellular events.