Depletion of Rho1 in adjacent cells is required to disrupt AJs, but decreased apical tension is cell autonomous. (a and b) Confocal immunofluorescent localization of DE-cadherin (DE-cad) in a single PEC clone (a and a′) and multiple cell clones (b and b′) expressing Rho1-RNAi (marked with GFP). Arrows in b′ identify intact AJs between a clonal cell and wild-type cell, and arrowheads identify disrupted AJs between two adjacent clonal cells. (c and c′) Apical (c) and lateral (c′) optical sections of DE-cadherin immunofluorescent localization in a Rho1-RNAi clonal cell. The yellow line (c) identifies where the lateral section (c′) was taken. The asterisks mark analogous cells in adjacent ommatidia. The arrow (c′) identifies a Rho1-RNAi clone. (d–d″) Confocal immunofluorescent localization of DE-cadherin (d and d′) and Rho1 (d″) in Rho172 (Rho1 null) MARCM clones (clonal cells are GFP positive). (e–e′″) Confocal immunofluorescent localization of DE-cadherin (e–e″) and phalloidin staining (F-actin; e″ and e′″) in Rho172 MARCM clones. (d and e) Arrows identify clonal cells, and arrowheads identify disrupted AJs between two clonal cells. (f–f″) Confocal immunofluorescent localization of DE-cadherin (f and f′) and Rho1 (f″) in Rho172 MARCM pupal eye clones overexpressing Rho1. Arrows identify cells with rescued apical profiles, and arrowheads identify rescued AJs between clonal cells. Bars, 10 µm.