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. 2018 Sep 26;115(42):10684–10689. doi: 10.1073/pnas.1807325115

Fig. 1.

Fig. 1.

Hrb27C mutations are dominant suppressors of the aPKC overexpression phenotype in the Drosophila eye. (A and B) Confocal images of wing imaginal discs from third instar larvae expressing GFP (green or gray) in a stripe of cells along the anterior-posterior compartment boundary driven by dpp-Gal4 and white-RNAi (A) or aPKCζ* and white-RNAi (B). (C) Eye of a fly with one copy of the GMR-Gal4 transgene. (D) Eye of a fly with GMR-Gal4–driven overexpression of aPKCζ*. (EG) GMR>aPKCζ* flies also carrying one copy of the allele Hrb27CJ6, Hrb27CF2-1, or Df(2L)BSC108 (which deletes Hrb27C). (H) GMR>aPKCζ* fly coexpressing Hrb27C-RNAi (v16041). (I) Diagram of the Hrb27C protein depicting its functional domains and the location of the Hrb27CF2-1 and Hrb27CJ6 mutations. The gray bars at the C-terminal end mark the locations of epitopes recognized by the Hrb27C polyclonal antibodies. RRM, RNA-recognition motif.