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. 2017 Apr 1;144(7):1317–1327. doi: 10.1242/dev.140434

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© 2017. 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. 2. — Hyperproliferation due to Ad-Cre-mediated Ptch1 loss is not due to SMO activation. (A) Hematoxylin and Eosin-stained vehicle-treated (left panels) and IPI926-treated (right panels) unscratched (upper panels) and scratched (lower panels) uterine tissue, showing decidualization in the vehicle-treated scratched uterus only. (B) qPCR of Ptch1^+/+ and Ptch1^fl/fl outgrowths showing no significant changes in hedgehog activation, aside from upregulation of Ptch2. Unpaired t-test are used for statistics. Data are represented as 2^−dCt. (C) Ki67 and GFP co-stained vehicle-treated Ptch1^+/+ (upper left), vehicle-treated Ptch1^fl/fl (lower left), IPI926-treated Ptch1^+/+ (upper right) and IPI926-treated Ptch1^fl/fl ducts (lower right). (D) Quantification of the percentage of Ki67-positive cells by genotype, showing increased proliferation in vehicle and IPI926- treated mutant ducts relative to controls by paired t-test. (E,F) Confocal images of cyclin B1- stained Ptch1^+/+ and Ptch1^fl/fl ducts. (G) There is increased nuclear localization in Ptch1^fl/fl ducts compared with controls (paired t-test). The scatterplot shows data as mean±s.e.m. Boxplots show data as mean±s.e.m., with minimum and maximum values. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Scale bars: 50 µm in A,C; 10 µm in E,F.