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. 2015 Apr 9;6(4):e1713. doi: 10.1038/cddis.2015.85

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Wg signaling is required for the physiological functions of Bsk. Compared with wild-type clones in the wing pouch (a), puc loss-of-function clones show dramatically reduced size (b), which is fully rescued by RNAi knocking-down of pan (c). (d) Statistics of total clone areas in (a–c). For each genotype, at least 10 clones were analyzed. Three asterisks, P<0.001; n.s., P>0.05. Compared with the ptc-Gal4 control (e), knocking-down of puc along the A/P boundary results in a loss-of-ACV phenotype (f), which is significantly suppressed by knocking-down of wg (g) or expression of Sgg (h). (i) Statistics of the loss-of-ACV phenotype in (e–h) (e, 0.00%, n=301; f, 96.03%, n=126; g, 1.25%, n=240; h, 30.00%, n=100). Three asterisks, P<0.001