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. 2014 Aug;141(15):3003–3012. doi: 10.1242/dev.105924

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© 2014. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 3. — SHH signaling is disrupted in the developing face and brain of talpid² mutants. (A) qRT-PCR for SHH in frontonasal (FNP), maxillary (MXP) and mandibular (MNP) prominences in control and talpid² embryos; *P<0.05. Data are mean±s.e.m. (B) In situ hybridization for SHH in control (n=7) and talpid² (n=3) HH25 embryos. (C) qRT-PCR for PTC; *P<0.03. Data are mean±s.e.m. (D) In situ hybridization for PTC in control (n=7) and talpid² (n=3) HH25 embryos. (E) RNA-seq results for SHH, PTC, GLI2 and GLI3 expression. (F-K) In situ hybridization for SHH in control and talpid² embryos. (F,G) Dorsal view of control (n=11) and talpid² (n=9) HH10 embryos. (H-K) Frontal and lateral views of control (n=8) and talpid² (n=4) HH20 embryos. Dotted black lines in I,K represent the size of the expression domain in the control embryo (H,J). ZLI, zona limitans intrathalamica. Scale bars: 250 µm in B,D; 600 µm in F,G; 100 µm in H,I; 200 µm in J,K.