Figure 7
scrib shows genetic interaction with dlg in posterior patterning of the follicular epithelium. (A) Quantification of loss of the PFC fate and FC overaccumulation at the anterior. Heterozygous scrib2 increases the penetrance of loss of the PFC fate and overaccumulation of the AFCs in dlgm52/+; dlgRNAiegg chambers in which GR1-Gal4-driven expression of the dlgRNAitransgene is induced in all FCs heterozygous for dlgm52(** P < 0.01). (B) Egg chambers at stage 9 from wild type (a) and dlgm52/+; dlgRNAi; GR1-Gal4/scrib2 females (b, c) stained for β-gal (green in a, b; white in b'), nuclei (DAPI, blue), and Phalloidin (red in a, b and c). The specified PFCs can be visualized by the enhancer trap marker 998/12 in stage 9 wild type egg chamber (a). Loss of 998/12 expression is evident in most of the multilayered FCs at the posterior in dlgm52/+; dlgRNAi; GR1-Gal4/scrib2 egg chambers in which endogenous dlg is knockdowned in all FCs doubly heterozygous for dlgm52 and scrib2 (b, b'). In these mutant chambers, FC overaccumulation is also observed at the anterior (c).