acal is a Long Non-coding RNA in JNK Signaling in Epithelial Shape Changes during Drosophila Dorsal Closure
Figure 5
raw and acal act together to counteract JNK signaling.
(A) Wild type cuticle. (B) Cuticle phenotype of raw mutant embryo. (C) Genetic interaction between raw2 and acal5 mutants. raw-like phenotype is depicted in (B). In raw+/+; acal5/5 mutants a small percentage survives embryogenesis, and constitute the open space above the bar to amount to a hundred percent total. Number of animals analyzed: raw+/+,acal5/5 = 391, raw2/+,acal5/5 = 139, raw2/2,acal+/+ = 366, raw2/2,acal5/+ = 152, raw2/2,acal5/5 = 208. Significance was assessed with chi square tests. (D-E) acal in situ hybridization in raw2 mutants (n = 45; D) and heterozygous siblings (n = 106; E). Arrow in (E) points to decreased acal expression in the lateral epidermis. See also S5 Fig. (F-I) Scanning electron micrographs of dorsal views of adult thoraces, anterior is up. Scale bars are 100 μm. (F) UAS-acal/+ control, (G) pnr-gal4/+ control, and (H) over-expression of two UAS-acal copies. The white box in (H) is amplified in (I), depicting distances (red lines) measured to determine the thoracic cleft index, using anterior dorso-central (ADC) and posterior dorso-central (PDC) bristles as references (see Materials and Methods). (J) Percentage change of thoracic cleft index for different experimental conditions. Mean of 15 flies +/− SEM. Significance was calculated using ANOVA and Bonferroni correction.
