Figure 2. Loss of abl delays and disrupts the organization of adherens junctions between the photoreceptors.

Eye discs with abl clones were stained with anti-Arm (red) and anti-GFP (green) antibodies. Lack of GFP marks abl mutant clones in this and all other figures in this paper. Scale bars: 10 μm.

A-C) are confocal projections of all transverse sections, and D-K) are zoomed-in single transverse (D, F-G, I-J) or orthogonal (E, H, K) sections of the two adjacent ommatidia (outlined by white boxes in A-C) with the wild-type ommatidium outlined by a solid yellow circle/box and the abl mutant ommatidium outlined by a dashed yellow circle/box.

A, D-E) Arm expression appears reduced, but fairly normally patterned and localized in abl mutant ommatidia in a third instar disc.

B, F-H) At 24hr APF, the adherens junctions between the cone cells in abl mutant ommatidia appear normal (F). Arm enrichment between the abl mutant photoreceptor cells is clearly evident at this stage, although still mildly weaker and less tightly organized than wild type (G).

C, I-K) At 48hr APF, apical Arm enrichment is undetectable in abl mutant ommatidia (I) and has collapsed to the basal plane of the epithelium (J-K).

Supplementary Fig. 2 shows analogous phenotypes in the hypomorphic abl¹ allele.