Figure EV1. Knockdown of dpr12 results in regrowth phenotype and description of Dpr12 alleles used in the study, related to Fig 1.
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ALeft: Graphs depicting the normalized RNA expression levels of selected Dprs in WT γ‐KCs (black), and in γ‐KCs expressing EcRDN (green) or UNF‐RNAi (blue). *P < 0.05; Error bars indicate SEM; units on the y‐axis are arbitrary. Right: Confocal z‐projections of adult γ‐KCs expressing RNAi transgenes as indicated labeled with membrane‐bound GFP (mCD8‐GFP; CD8) driven by the γ‐specific Gal4 driver R71G10‐Gal4 (γ‐Gal4). Note that while R71G10 is consistently expressed in γ‐KCs, it is also expressed in α/β‐KCs in a stochastic manner.
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BA schematic representation of the Dpr12 locus showing introns (black line) and coding and non‐coding exons (red and gray, respectively). The location of Dpr12 gRNA (arrow), dpr12∆50‐81 mutation (arrow), dpr12 RNAiJF03210 (black lines connected with dashed lines), and MiMICMI01695 (arrowhead) is indicated. SA and SD are splice acceptor and donor sites, respectively. Recombination‐mediated cassette exchange was used to transform Dpr12MI01695 into Dpr12GFSTF.
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CA schematic representation of Dpr12 protein variants. Signal peptide (SP), Immunoglobulin (Ig), transmembrane (TM), and GPI anchor (GPI).
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DRanking of regrowth: Confocal z‐projections of adult γ‐KCs labeled with membrane‐bound GFP (mCD8‐GFP; CD8) driven by the γ‐specific Gal4 driver GMR71G10‐Gal4 (γ‐Gal4). Representative images of the regrowth defect severity (1 = strong, 2 = intermediate, 3 = weak, 4 = WT) described in Fig 1O. The arrowhead demarcates an unusually short β‐lobe; morphologically abnormal β‐lobes (either short, thin or absent) appear in approximately 40% of either dpr12 or DIP‐δ homozygous mutant brains. Since β‐lobe morphology is rescued by overexpressing a UAS‐Dpr12 transgene within γKCs, it is most likely a non‐cell‐autonomous defect, which is beyond the scope of this study. Asterisk demarcates the distal tip of the γ‐lobe. Green is CD8‐GFP; magenta is FasII staining. Scale bar is 20 µm.