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. Author manuscript; available in PMC: 2014 Sep 15.
Published in final edited form as: Dev Biol. 2013 Jul 11;381(2):482–490. doi: 10.1016/j.ydbio.2013.07.001

Fig. 6. ewg acts genetically upstream of warts and melted.

Fig. 6

(A–H) Confocal images of adult retinas stained with antibodies for Rh5 (blue) and Rh6 (red). (A) Over-expression of melted driven by IGMR-Gal4 results in Rh5 expressed in all R8s. (B) In ewgl1; IGMR>melted flies, overexpression of melted suppresses the ewgl1 phenotype, leading to Rh5 expression in all R8s. (C) In a warts mutant, all R8s are converted to pR8 expressing Rh5. (D) ewgl1; warts− double mutants show Rh5 expression in all R8s. (E) Overexpression of a dominant negative form of Merlin (merDN) in all PRs leads to expression of Rh5 in all R8s. (F) A merDN;ewg double mutants show Rh5 expression in all R8s. (G) Over-expression of yki driven by GMR causes Rh5 expression in all R8s. (H) Over-expression of yki in ewgl1mutants suppresses the ewg phenotype and leads to Rh5 expression in all R8s. (I) Model of ewg interaction with the Warts-Melted feedback loop. ewg acts upstream of melted to promote its expression, allowing expression of Rh5 in pR8s. ewg might also be required to repress the Hippo pathway, leading to Rh5 expression.