Correction: Prp8 regulates oncogene-induced hyperplastic growth in Drosophila

There was an error in Development (2018) 145, dev162156 (doi:10.1242/dev.162156).

The authors contacted the journal to inform us that panels B and C of Fig. 1 had been inadvertently switched during the proof correction process. We have been able to verify this through examination of files provided for Fig. 1 at the time of article acceptance. The corrected Fig. 1 is shown below.

Fig. 1.

(corrected). prp8 knockdown regulates growth during development and tumourigenesis. (A-D) Images of third instar larvae showing distribution of GFP expression induced in the eye discs and optic lobes of control (A), RasV¹² (B), prp8^RNAi (C) and RasV¹²; prp8^RNAi (D). (E-H) Confocal micrographs of eye imaginal discs from third instar larvae of the indicated genotypes, stained with anti-GFP (green) and the DNA marker Hoechst (blue). When compared with controls (A and E), prp8^RNAi decreased the GFP-positive area in whole larvae (C) and caused eye disc hypoplasia (G). When combined with RasV¹² expression, prp8 depletion led to a decrease in the GFP-positive area (D) and partially rescued eye disc morphology (H), when compared with RasV¹² alone (B and F). (I) Quantification of frequency of phenotypes observed with all prp8^RNAi lines used in this study (n>60). (J-M) xy sections of third instar eye discs containing clones that were induced with the MARCM system. MARCM FRT42D blank clones (J), UAS-RasV¹² MARCM clones (K), prp8^KG03188 MARCM clones (L) and prp8^KG03188; UASRasV¹² MARCM clones (M) are marked by GFP (green). DNA is stained with Hoechst (blue). Scale bars: 1 mm in A-D; 200 µm in E-H; 100 µm in J-M.

The authors apologise for this error, which does not impact the results and conclusions of the paper.