Ft ICD recruits Dachs and influences its abundance. (A) CRISPR-Cas9 induced ft^ΔICD mutant. The target sequence (green line), PAM site (green box), and transmembrane domain (TM; blue letters) are shown. The resulting 4-bp deletion led to a premature stop codon after the transmembrane domain. The altered amino acids are shown in red letters. (B) App:YFP is increased in junctional puncta in ft⁶¹ mutant cells. (C) Dachs:GFP is increased at the junctional puncta in ft⁶¹ mutant clones. Mutant clones are marked by the absence of ubi-RFP. (D) Phosphorylation of wild-type Ft and Ft^sum by Dco in S2 cells. Dco WT promotes phosphorylation of Ft. The Ft^sum is less phosphorylated by Dco. (E) Efficacy of app and dlish dsRNAs in S2 cells. Both proteins are strongly reduced by cotransfection of dsRNA. (F) Ed:Ft:Flag recruits Dachs:GFP to cell–cell contacts in app and dlish depleted cells. (G) Ed:FtΔ6-C:Flag fails to recruit Dachs:GFP in app and dlish depleted cells. (H) Ed: FtΔN-6:Flag fails to recruit Dachs:GFP in app and dlish depleted cells. Scale bar, 5 µm (B and C) 1 µm (F–H). Yellow arrows in F–H indicate cell contacts. Source data are available for this figure: SourceData FS4.