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. 2019 Nov 7;15(11):e1008454. doi: 10.1371/journal.pgen.1008454

Fig 2. Loss of α-Cat activates JNK pathway and Yki.

Fig 2

(A) Activation of the JNK transcriptional reporter puc-LacZ is seen when α-Cat is depleted in the PC. The strong reduction of the PC in α-Cat-RNAi(1) and puc-LacZ compared to α-Cat-RNAi(1) wing discs (see Fig 1C) indicates a genetic interaction between α-Cat-RNAi(1) and puc-LacZ. The loss of the PC can be rescued by expression of p35 or removal of one copy of Rho1. Scale bars, 100 μm. (B) Schematic illustrating the relationship between Puc and JNK. The phosphatase Puc dephosphorylates and therefore deactivates the JNK kinase. The presence of the puc mutant allele puc-lacZ is predicted to hyper-activate JNK in conjunction with a KD of α-Cat, which causes enhanced cell death as observed in (A). (C) Elevated expression of the Yki transcriptional reporter ex-lacZ is observed upon KD of α-Cat in the absence or presence of p35. Tissue overgrowth is suppressed through the addition of a null mutant copy of yki (ykiB5). Scale bars, 100 μm. (D) Quantification of wing disc area in flies of indicated genotypes. Two-tailed, unpaired t-test; ns (P>0.05), ****(P≤0.0001), ***(P = 0.0003).