Fig. 5.

Ets21c cooperates with Ras^V12 to promote tumor growth, increase MMP1 expression and delay development. (A-K) Co-expression of ras^V12 with ets21c^LONG caused noticeable expansion of the GFP⁺ clonal area in EAD already on day 6 AEL (E,J). Nevertheless, photoreceptor differentiation marked by ELAV still occurred (E). Neither fos^WT nor α- or β-ftz-f1 overexpression was sufficient to enhance clonal tumor growth when combined with ras^V12 (B-D). Similar to ras^V12 mosaic EAD (F), clones co-expressing ras^V12 with fos^WT (G), α-ftz-f1 (H), β-ftz-f1 (I) or ets21c^LONG (J) showed only moderate enhancement of MMP1 levels on day 6 AEL. On day 9 AEL, ras^V12ets21c^LONG clones showed massive enrichment of MMP1 signal (K). Images show EAD as projections of multiple confocal sections. Scale bars: 100 µm (A-K). (L) ras^V12α-ftz-f1 and ras^V12β-ftz-f1 larvae pupated slightly later compared with ras^V12 alone or ras^V12fos^WT (P<0.0001). In contrast, pupation of ras^V12ets21c^LONG larvae was delayed by 2 days (P<0.0001). Inhibition of JNK (ras^V12ets21c^LONGbsk^DN) further exacerbated the delay, arresting 29% of the tumor-bearing animals at the larval stage (P<0.0001). The graph shows the cumulative percentage of pupae forming over time.