Model depicting the influence of Cdon mutation and ethanol exposure on Shh signaling activity in the developing eye. Model depicting the influence of Cdon.

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Model depicting the influence of Cdon mutation and ethanol exposure on Shh signaling activity in the developing eye. Model depicting the influence of Cdon mutation and ethanol exposure on Shh signaling activity in the developing eye. (A) In wild-type embryos (E14.5), the binding of Shh to Cdon and Ptch1 releases the inhibition on smoothened (Smo), facilitating the transcription by Gli activator (GliA) of target genes involved in RPC proliferation. (B) In the eyes of 129S6.Cdon−/− embryos, there is persistent inhibition of Smo by Ptch1, even in the presence of Shh, causing Gli repressor (GliR) to block transcription of genes involved in RPC proliferation, resulting in precocious RPC differentiation. (C) Ethanol exposure at E8.0 interferes with Shh signaling in the eye through a variety of proposed mechanisms. The lengthy delay between ethanol exposure (E8.0) and its negative effects on Shh signaling activity (E14.5), suggests that the epigenetic landscape of Shh target genes might be modified to suppress RPC proliferation. (D) Cdon mutation or ethanol exposure at E8.0 impedes Shh signaling activity in RPCs resulting in optic nerve hypoplasia. Benjamin M. Kahn et al. Dis. Model. Mech. 2017;10:29-37 © 2017. Published by The Company of Biologists Ltd