Figure 3. Mutations in lgd cause disruptions in Notch trafficking.

(A–A‴) An lgd^d7 mutant clone in a third instar wing disc, indicated by the absence of ubiGFP (blue), stained for α-N^ICD (green in A and A‴, gray in A′) and α-Hrs (red in A and A‴, gray in A″). N^ICD and Hrs accumulated together in lgd mutant cells (arrowhead). (B–B′) An lgd^d7 mutant clone in a third instar wing disc, indicated by the absence of ubiGFP (blue) stained for α-N^ECD (green in B, gray in B′). The arrowhead indicates one of the subcellular puncta that shows accumulation of the extracellular part of the Notch protein. (C–C′) vps25, UAS-P35 MARCM mutant clones in the third instar wing disc, indicated by the presence of UAS-GFP (blue), stained for α-Hrs (red in C, gray in C′). The arrowhead indicates one of the subcellular puncta that expressed Hrs. (D–D‴) vps25 MARCM mutant clones in a third instar wing disc, indicated by the presence of UAS-GFP (blue) stained for α-N^ICD (green in D and D‴, gray in D′) and α-Lgd (red in D and D‴, gray in D″). Both N^ICD and Lgd protein accumulate in the vps25 mutant cells. (E–E′) An hrs^D28 mutant clone in a third instar wing disc, indicated by the absence of ubiGFP (blue), stained for α-N^ICD (green in E and E‴ and gray in E′) and α-Lgd (red in E and E‴ gray in E″). N^ICD staining accumulated in the mutant cells, but there was no change in Lgd protein levels or localization within the clone compared to wild-type cells.