Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

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

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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.

PMC Copyright notice

Fig. 3. — Silencing β-catenin partially rescues the Ck1α^RNAi-induced wound closure defect. (A) Schematic of the experimental design/temperature shift regimen for using Gal80^ts to inducibly express UAS-dependent transgenes in the larval epidermis. (B-E) Dissected epidermal whole mounts of pinch-wounded third instar larvae expressing Gal80^ts transgene driven by a tubulin promoter, UAS-DsRed2Nuc (nuclei, magenta) via the e22c-Gal4 driver, and the indicated transgenes. Cell boundaries were immunostained using anti-Fasciclin III antibodies (green). (B) Control^RNAi, (C) UAS-Ck1α^RNAi#3 and control^RNAi, (D) UAS-β-catenin^RNAi, (E) Ck1α^RNAi#3 and UAS-β-catenin^RNAi. Scale bar: 100 μm. (F) Quantitation of the percentage of open wounds in larvae expressing indicated transgenes via the e22c-Gal4 driver. Each dot represents one set of n≥8 for each genotype. Data are mean±s.e.m. *P<0.05, **P<0.01 (one-way ANOVA).