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. 2019 Oct 2;146(20):dev175133. doi: 10.1242/dev.175133

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© 2019. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 4. — The epidermal Ck1α^RNAi-induced wound-closure defect is E-cadherin dependent and Wnt signaling independent. (A) Schematic of the experimental design/temperature shift regimen for using Gal80^ts to inducibly express UAS-dependent transgenes in the larval epidermis. (B-G) Dissected epidermal whole mounts of pinch-wounded larvae expressing the Gal80^ts transgene driven by a tubulin promoter, UAS-DsRed2Nuc (nuclei, magenta) via the e22c-Gal4 driver, and the indicated transgenes 24 h after wounding. Cell boundaries were immunostained using anti-Fasciclin III antibodies (green). (B) Control^RNAi, (C) Ck1α^RNAi#3 and control^RNAi, (D) E-cad^RNAi, (E) Ck1α^RNAi#3 and E-cad^RNAi, (F) UAS-TCF^RNAi, (G) Ck1α^RNAi and UAS-TCF^RNAi. Scale bar: 100 μm. (H) Quantitation of the percentage of open wounds in third instar larvae expressing the indicated transgenes via the e22c-Gal4 driver. Each dot represents one set of n≥8 larvae for each genotype. Data are mean±s.e.m. **P<0.01; ns, not significant (one-way ANOVA).