Figure 4. Ets21C cooperates with the JNK pathway to activate target genes.

(a) Blocking the JNK pathway by expressing bsk^DN in Ras^V12 dlg^RNAi (RDi) tumors that overexpress Ets21C abrogates the induction of Mmp1, Pvf1 and upd1 expression as assessed by qRT-PCR. (b) A similar effect is observed if the JNK pathway is blocked by knocking down jun and fos. Error bars indicate SD. (c) Ets21C physically interacts with Jun (second lane) or Fos (third lane). Kc167 cells were transfected with the transgenes indicated, together with tub-Gal4 and dTak1 to activate the JNK pathway. Anti-HA immunoprecipitates were immunoblotted first with anti-FLAG or anti-GFP antibodies (parts of the blot below 35 kDa). GFP was used as a negative control. After stripping, the same blot was incubated with anti-HA antibodies. (d) Model of Ets21C action: Ets21C is expressed in response to JNK pathway activation as a consequence of loss of polarity. Once Ets21C is expressed, it associates with AP-1 and together they drive the expression of target genes critical for tumor growth and invasion such as Mmp1, Pvf1 and upd1.