Fig. 8

Slik/STK10 prevents physiological JNK-mediated cell death. Light micrographs of Drosophila adult wings (A–D) and fluorescence micrographs of third instar larval wing discs (F–I, K–L) are shown. RNAi-mediated down-regulation of scrib along the A/P compartment boundary by ptc-Gal4 triggered the loss-of-ACV phenotype in adult wings (B), which was resulted from cell death in larval wing discs (G). Both phenotypes were inhibited by expressing Slik or STK10 (C–D, H–I). The bottom panels show high magnification views of the boxed areas in upper panels (A–D). Importantly, ptc > scrib-IR-induced cell death (K) was enhanced in heterozygous slik mutants (L). Statistical analysis of the presence of ACV in adult wings (E, n = 15 for each genotype) and cell death number in wing discs (J and M, n = 10 for each genotype) were shown. (N) Immunoblot analysis of p-JNK and total JNK protein level in SW480 cells treated by nonspecific siRNA (siCtrl) or two independent siRNA targeting STK10 (referred to as siSTK10-1 and siSTK10-2). p-JNK protein level was increased upon STK10 knockdown, while total JNK protein level remained unchanged. One-way ANOVA with Bonferroni multiple-comparison test and unpaired two tailed t-test were used to compute P-values, ****p < 0.0001, ***p < 0.001, **p < 0.01, *P < 0.05. See the supplementary material for detailed genotypes. Scale bar: 100 μm in A–D (upper panels), F–I and K–L, 50 μm in A–D (lower panels)