Fig. 4
From: Slik maintains tissue homeostasis by preventing JNK-mediated apoptosis
Slik acts upstream of or in parallel to Hep to adjust JNK-dependent apoptotic cell death. Fluorescence micrographs of third instar larval wing discs are shown (A–J). Compared with the control (A), RNAi-mediated down-regulation of slik along the A/P compartment boundary by ptc-Gal4 induced obvious cell death (B), which was suppressed by depletion of hep (G) or bsk (H), or expressing a dominant-negative form of Bsk (I) or Puc (J), but remained unaffected by expressing RNAi of lacZ (C), egr (D), dTRAF2 (E) or dTAK1 (F). Merged fluorescence micrographs of third instar larval wing discs are shown (L–P). Compared with the control (L), loss of slik-induced apoptosis M was blocked by expressing hep RNAi O or BskDN (P), but not by egr RNAi (N). Statistical analysis of the AO positive cell numbers (K, n = 10 for each genotype) and cleaved Dcp-1 (cDcp-1) activity (Q, n = 10 for each genotype) in wing discs are shown. One-way ANOVA with Bonferroni multiple-comparison test was used to compute P-values, ****P < 0.0001, n.s indicates not significant. See the supplementary material for detailed genotypes. Scale bar: 50 μm