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. 2015 Feb 26;4:e03189. doi: 10.7554/eLife.03189

Figure 4. JNK-Dependent transcription is necessary for overgrowth and upd3.3 activation upon polarity loss.

WT wing discs (A) do not express either the JNK target Mmp1 or upd3.3LacZ (A′). Expression of dlgRNAi promotes overgrowth and disorganization (B), as well as Mmp1 and upd3.3LacZ upregulation (B′). Inhibiting AP-1 transcription with either JNKDN or FosDN restores normal disc size and architecture (C and D), and abrogates Mmp1 and upd3.3LacZ expression (C′ and D′). WT discs segregate apical aPKC and basolateral Scrib (E). dlgRNAi expression leads to apical domain expansion and co-localization of aPKC and Scrib (F, arrowheads). Co-expressing JNKDN and dlgRNAi restores the separation of aPKC and Scrib (G). Activation of JNK is sufficient, when apoptosis is blocked with miRGH, to drive upd3.3LacZ, Mmp1 and overgrowth but not to alter polarity (H and I). Scale bars: A–D, H: 100 μm, E–G, I: 10 μm.

DOI: http://dx.doi.org/10.7554/eLife.03189.010

Figure 4.

Figure 4—figure supplement 1. Inhibitor constructs do not significantly affect WT tissue growth and viability.

Figure 4—figure supplement 1.

(A–B) Blocking JNK activity with JNKDN or FosDN (C) has no effect on normal growth or tissue architecture, relative to wild-type. Expression of miRGH does not affect normal tissue architecture or growth (D). Knockdown of Yki promotes mild architecture defects (E), while BrmDN expression has no phenotype (F). For all panels, transgenes were expressed in the dorsal wing pouch with the ms1096-GAL4 driver. Scale bar: 100 μm.
DOI: http://dx.doi.org/10.7554/eLife.03189.011
Figure 4—figure supplement 2. Quantification of upd3.3LacZ staining.

Figure 4—figure supplement 2.

(A) Expression of dlgRNAi increases upd3.3LacZ fluorescence, which is suppressed by blocking JNK or Trx activity. (B) Expression of aPKCact stimulates upd3.3LacZ in a JNK-independent, but Yki-dependent manner. (C). Hyperactivation of Yki or JNK activity upregulates upd3.3LacZ expression. (D) Alone, expression of aPKCmild, ph-pRNAi, or JNKKWT does not activate upd3.3LacZ; however, co-expression of aPKCmild with ph-pRNAi or JNKKWT drives upd3.3LacZ. (**p < 0.001; n.s. = not significant).
DOI: http://dx.doi.org/10.7554/eLife.03189.012
Figure 4—figure supplement 3. Neoplasia induced by scrib loss is also dependent on JAK-STAT, JNK, and Yki pathway activity.

Figure 4—figure supplement 3.

(A–C) Reducing JAK-STAT activity with DomeDN or Socs36E attenuates scribIR-mediated overgrowth. (D–H) Blocking JNK pathway activation by depletion of the JNK kinase hep or overexpression of JNKDN suppresses the overproliferation, architecture defects and upd3.3LacZ activation induced by scrib loss. (I and J) Yki is necessary for neoplastic overgrowth of scrib tissue. Scale bar: 100 μm.
DOI: http://dx.doi.org/10.7554/eLife.03189.013