acal is a Long Non-coding RNA in JNK Signaling in Epithelial Shape Changes during Drosophila Dorsal Closure
Figure 6
Cka is downstream of raw and acal.
(A) Genetic interaction between Cka and acal mutants. Number of animals analyzed: Cka+/+,acal2/2 = 192, Cka1/+,acal2/2 = 219, Cka+/+,acal5/5 = 391, Cka1/+,acal5/5 = 171. (B) Cka relative expression in wild type and mutant embryos, as determined by qPCR. (C) Expression of a heat-shock inducible Cka transgene results in DC defects. Number of animals analyzed: yw, 25°C = 526, yw, 29°C = 591, HS-Cka, 25°C = 2006, HS-Cka, 29°C = 3227. (D) Cka expression increase due to heat shock in hs-Cka flies was confirmed by qPCR. For (A,C) embryos surviving embryogenesis represent the open space above the bar to amount to one hundred percent total of embryos analyzed. Chi square tests were used to calculate significance. For (B,D) represents the means of three independent experiments run twice +/− SEM. Significance was assessed using Student’s t test. (E-H) dpp in situ hybridization experiments, showing JNK-induced dpp expression (arrows). (E) Wild type embryo. (F) raw1/1,en-gal4/+ control, showing dpp ectopic activation (arrow). (G) Expression of UAS-rawRA with en-gal 4, which expresses gal 4 at posterior compartments of each segment. Arrowheads show cell-autonomous suppression of dpp ectopic expression. (H) Silencing of Cka with an RNAi construct (UAS-Cka-IR) under en-gal 4 also suppresses dpp ectopic expression in posterior compartments of raw1 mutants (arrowheads).
