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. 2012 Dec 20;6(2):537–543. doi: 10.1242/dmm.010132

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© 2013. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-ncsa/ 3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 1. — NODAL signal inhibition by SB-505124 treatment leads to severe forebrain defects; the dose-response relationship is nonlinear. (A) Ventral views of chick embryo heads at stage 12. Control embryos (n=150) were treated with DMSO (Aa, Ae, Ai). Other embryos were treated with one of a series of SB-505124 concentrations (10-75 μM) between stage 4 and stage 6 (n=317). Resulting phenotypes were classified into three categories according to morphology and in situ hybridization for Pax6 (n=111) (Aa-Ad), Shh (n=107) (Ae-Ah) and Nkx2.1 (n=99) (Ai-Al). The order of increasing severity was: category 1, category 2 and category 3. Arrowheads show the downregulation of Shh (Ag) and Nkx2-1 (Ak) expression in the ventral forebrain. (B) Distribution of the phenotypes of stage 4+ embryos treated with one of a series of SB-505124 concentrations: 10 μM (n=15), 25 μM (n=20), 50 μM (n=22) or 75 μM (n=26). (C) Distribution of the phenotypes of embryos treated with 50 μM SB-505124 starting at various stages: from stage 4 (n=40), stage 4+ (n=22), stage 5 (n=29) and stage 6 (n=16). OV, optic vesicles; T, telencephalon; T*, non-fused telencephalon; Cat, category.