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. 2015 Oct 6;11(10):e1005576. doi: 10.1371/journal.pgen.1005576

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© 2015 Schleede, Blair

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 4 — (A) Complete loss of the PCV in cv ⁷⁰ wing. (B) Ectopic venation in en-Gal4 UAS-myc-gyc76C / + wing. (C) Loss of PCV and lack of ectopic venation in cv ⁷⁰ / Y; en-Gal4 UAS-myc-gyc76C / + wing. (D) PCV disruption in A9-Gal4/+; UAS-gyc76C-RNAi (VDRC v6552) / + wing. (E,F) Rescue of the PCV disruption normally caused by gyc76C knockdown by expression of an activated form of Tld in an A9-Gal4 / +; UAS-tld ^A53 / +; UAS-gyc76C-RNAi / + wing (E), or by overexpression sog, cv and cv-2 in A9-Gal4 / cv ^EP1349; cv-2 ^EP1103 / +; UAS-sog / UAS-gyc76C-RNAi wing (F). (G) PCV loss in en-Gal4 / +; UAS-sog / + wing. (H) Rescue of PCV loss by Gyc76C overexpression in en-Gal4 UAS-myc-gyc76C / +; UAS-sog wing.