Fig. 5

RA and TH have reciprocal interactions on caudal neural crest development that are mediated by RXR. Treatment of Tg(sox10::EGFP) embryos injected with control MO with 1 nM RA starting at 12 hpf had minimal teratogenic effects (B) vs. control media (A). Treatment with RXR antagonist, 10 nM UVI3003 in the absence (C) or presence of 1 nM RA (D) had minimal affect on cranial neural crest development. MO knockdown of Thraa caused malformation of ceratohyal and Meckels cartilage formation (E) which was rescued by 1 nM RA (F) starting at 12 hpf. In contrast, treatment with UVI3003 (10 nM) at 12 hpf further inhibited Meckels, ceratohyal, and posterior PA cartilage (G) and abrogated the effect of exogenous RA (H) on Thraa MO knockdowns. MO knockdown of Dio3 inhibited posterior PA formation (I) which was improved by exogenous RA (1 nM, J) starting at 12 hpf. 10 nM UVI3003 starting at 12 hpf improved posterior pharyngeal arch and ceratohyal cartilage in Dio3 MO knockdowns (K), however, co-treatment with 10 nM UVI3003 and 1 nM RA completely suppressed pharyngeal arch and jaw development (L). Scale bar=100 µm.