Fig. 3.

PIP2 levels control polarized BM deposition. (A, A′) Lg section through WT FCs (tj–Gal4) expressing Pcan–GFP (green), stained for F-Actin (red) and DNA (blue). (B, B′) Lg section through the FC layer of an egg chamber containing PI4KIIIα^GS27 clones, marked by the absence of intracellular GFP, coexpressing Coll IV–GFP (green) and stained for F-Actin (red) and DNA (blue). Clonal boundaries are indicated by a dashed line. WT and −/− homozygous FCs are specified. In PI4KIIIα mutant FCs, BM proteins accumulate apically in aggregates. (C, C′) Lg section through FCs expressing Pcan–GFP (green), stained for F-Actin (red) and DNA (blue), and expressing an RNAi construct against sktl (PIP5K) using tj–Gal4. The knockdown of PIP5K leads to the apical localization of Pcan–GFP. (D, D′) Lg section through the FC layer of an egg chamber containing PTEN^C494 clones, marked by the absence of intracellular GFP, coexpressing Pcan–GFP (green) and stained for F-Actin (red) and DNA (blue). In PTEN mutant FCs, Pcan–GFP accumulates apically in aggregates. Together, these data indicate that PIP2 controls the polarized secretion of BM proteins. (Bars, 10 μm.)