Fig. 3
From: Notch signals modulate lgl mediated tumorigenesis by the activation of JNK signaling
Nact/lgl-IR tumor induces cell death. Fluorescent micrographs of wing imaginal discs are shown. Acridine orange-staining in wild-type (a), Nact over-expressed (b), lgl-IR over-expressed (c) and both Nact/lgl-IR coexpressed (d) wing discs are shown. Expression of cleaved caspase 3 in wild-type (f), Nact over-expressed (g), lgl-IR over-expressed (h) are shown. i Nact/lgl-IR coexpressed wing disc shows upregulation in cleaved caspase 3 expression. MMP1 expression in wild-type (k), Nact overexpressed (l), lgl-IR overexpressed (m) are shown. n Nact/lgl-IR wing disc shows massive upregulation in MMP1 expression. Blocking cell death in Nact/lgl-IR tissues by expressing UAS-p35 leads to absence of acridine orange positive cells (e) and cleaved caspase-3 marked cells (j); whereas the expression of MMP1 is found to be unaltered (o). p Intensity per unit area for acridine orange shows that there is significant amount of upregulation of acridine orange-positive cells in Nact/lgl-IR wing disc. q Intensity per unit area for caspase staining shows that the Nact/lgl-IR wing disc contains significantly upregulated level of caspase activity than that of wild-type, lgl-IR and Nact wing discs. r Wing disc size analyses show that the disc size is increased when p35 is expressed in the background of Nact/lgl-IR, as compared to Nact/lgl-IR. Analysis of data for intensity profiling was done using two-way ANOVA with Tukey’s multiple comparison test; data represents mean ± SEM (***p < 0.001; **p < 0.01 and ns p > 0.05. Analysis of data for wing disc size was done using Unpaired t test with Welch’s correction; data represents mean ± SEM *p < 0.05). All wing discs are oriented with dorsal to the top and posterior to the right. Scale bars: 100 µm for (a–e), and 50 µm for (f–j, k–o)