Figure 1.

AVE displacement and anterior neurectoderm induction occur normally in the absence of huntingtin. Whole mount in situ hybridization analysis of Otx2 (A,B) and Hesx (C-F) in E7.5 normal (A,C,E) and mutant (B,D,F) embryos reveals that neuroectoderm and anterior visceral endoderm (AVE) develop normally in huntingtin deficient embryos, although the neuroectoderm expression domain is reduced. Asymmetrical expression of Hesx in mutant embryos (F) suggests that left-right transcriptional control is maintained. Hnf3β expression in the definitive endoderm extends around the distal tip and is reduced in the AVE (*) in both normal (G,I) and mutant embryos (H,J). Taken together, these results suggest normal ectoderm and endoderm induction and localization in Hdhex4/5/Hdhex4/5 embryos. Embryos are shown in lateral views, with anterior to the left in all pictures with the exception of E and F. Embryos are viewed from the anterior aspect in E and F.

Woda et al. BMC Developmental Biology 2005 5:17   doi:10.1186/1471-213X-5-17
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