Egg chamber elongation requires a functional WIRS. (A) Quantification of egg morphology defects of indicated genotypes. Scatterplot shows the egg index which represents the quotient of length divided by width; n = 100. **, P < 0.001; ***, P < 0.0001; and n.s., not significant (ANOVA). Please note that there are no significant differences between the wild-type and the Gal4 drivers alone. (B) Quantification of the frequency of round eggs of the two indicated genotypes. ***, P < 0.001 (t test). n = 4 independent experiments; in total, 1,304 wild-type eggs and 2,254 AbiΔWIRS eggs were analyzed. (C and D) Bright-field micrographs of Drosophila eggs of abi mutant females either rescued by reexpression of (C) a wild-type Abi (Abi-WT) transgene or (D) an Abi mutant transgene with a disrupted WIRS binding surface (AbiΔWIRS). Bars, 150 µm. (E) Confocal images were taken from the basal surface of stage 7–8 egg chambers of indicated genotypes. F-actin was visualized with phalloidin. Bars, 10 µm. (F) Quantification of the orientation of basal actin bundles in Abi-WT, AbiΔWIRS and fat2 mutant egg chambers (n = 13). Rose plots show density distribution of local angles of actin bundles (calculated using OrientationJ). The measured angles range between −90° and 90°. In wild type, basal actin bundles are orientated perpendicular to the A-P axis (−90° and 90°).