Figures
The figure legends for Figs. 5 and 6 are incorrectly switched. The figure legend that appears with Fig. 6 should be the figure legend accompanying Fig. 5, and the figure legend that appears with Fig. 6 should be the figure legend accompanying Fig. 5. The images appear in the correct order. The authors have provided Fig. 5 and Fig. 6 with the correct figure legends here.
(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).
(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.
Reference
Citation: The PLOS Genetics Staff (2015) Correction: acal Is a Long Non-coding RNA in JNK Signaling in Epithelial Shape Changes during Drosophila Dorsal Closure. PLoS Genet 11(4): e1005138. https://doi.org/10.1371/journal.pgen.1005138
Published: April 10, 2015
Copyright: © 2015 The PLOS Genetics Staff. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited