acal is a Long Non-coding RNA in JNK Signaling in Epithelial Shape Changes during Drosophila Dorsal Closure
Figure 1
Molecular and genetic characterization of acal mutants.
(A-L) Cuticular analysis of DC defects. In all figures, embryos are shown in a lateral view, with dorsal up and anterior left. Arrowheads show extent of cuticular holes. (A) Wild type cuticle. (B-D) bsk1 (JNK), Cka1, and aop1 mutant phenotypes. (E-L) acal mutants. (M-M’’) Schematic representation of the acal locus. (M) Deficiencies used to map acal mutants to the intergenic region between lola and psq (for simplicity, other genes are not depicted). Boxed area in (M) is amplified in (M’). (M’) The genomic rescue construct,178D09, spans the full acal genomic region, CR45135, and a small part of lola 5’. Boxed area in (M’) is amplified in (M’’). (M’’) Parental insertion P{KG09113} for acal1 and acal2 and insertion site of acal6 are shown. Molecular lesions of acal1 and acal2 are highlighted in bold. A putative poly-adenylation site is also depicted. Primer pairs numbers and amplicons used to sequence mutant alleles are also depicted. (N) A genomic rescue transgene significantly suppresses acal DC mutant phenotypes. Only mutant embryos with cuticle defects are shown, mutants surviving embryogenesis are not depicted (and constitute the open space above bars to amount to a hundred percent). In this and all figures, unless noted, mutant embryos were selected by lack of GFP expression, present in control embryos (possessing balancer chromosomes that express GFP). Number of animals analyzed: acal1/1 = 217, acal1/1;178D09 = 314, acal2/2 = 192, acal2/2;178D09 = 159. Chi square tests were used to assess significance. (O) Similarity tree of acal homologs among some sequenced Drosophilids. Bootstrap values are shown. Further genetic characterization is shown in S1 Fig.
