CK1-γ/gish and PCP effector mwh function in a genetically independent manner to restrict trichome formation. (A and B) The FRT82-gish^e01759 mutant clone (A) is dominantly enhanced by the multiple wing hairs (mwh¹)–null allele (B). (C) Wing hair number defects in D, E, and G–L were scored as a percentage of the total cells in the red highlighted region (D, E, and G–L are representative images of a smaller region within the red area). (D and E) mwh¹/mwh¹-null phenotype is enhanced by en-Gal4 UAS-gish^IR expression. (F) The quantification of results from D and E is represented. (G and H) The en-Gal4 UAS-gish^IR phenotype is strongly suppressed by coexpression of UAS-mwh. (I and J) UAS-mwh^IR was partially suppressed by UAS-myc-gish^WT coexpression. (K and L) Coexpression of UAS-myc-gish^KD, kinase-dead (KD; K), or the truncated/ubiquitously localized UAS-myc-gish^ΔC (L) failed to rescue the phenotype. (M) The quantification of results is represented. Error bars indicate SDs; unpaired t tests were performed on three independent animals (*, P < 0.05; ***, P < 0.001). WT, wild type. Bars: (A, B, and D–L) 25 µm; (C) 250 µm.