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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. 3. — Simultaneous partial inhibition of NODAL and SHH causes HPE-like anterior neural defects in chick embryo. (A) Ventral views of chick embryo heads at stage 12. Embryos were treated with SB-505124 (25 μM) and cyclopamine (0.006 μM) at stage 4+ (n=187). Three phenotypes were distinguished using Pax6 in situ hybridization. The order of increasing severity was: category I*, category II* and category III*. (B) Phenotype distributions among embryos treated with cyclopamine (n=52), SB-505124 (n=59) or both (n=76) at stage 4+. The asterisks show the significant cumulative effect of the double treatment leading to the HPE-like phenotype (*P=4×10⁻⁴). OV, optic vesicles; OV*, single optic vesicle; T, telencephalon; Cat, category.