Polarized actin-rich protrusions depend on WRC function. (A) Follicle cell–specific RNAi-mediated knockdown of sra-1 completely eliminates cellular protrusions. LifeAct-EGFP is more evenly distributed across the cell cortex. Time intervals are indicated. Bars, 5 µm. (B) Confocal image from the basal surface of a wave mosaic egg chamber (stage 7) shows that mutant cells (positively marked by CD8-GFP expression, blue) completely lack actin-rich protrusions (F-actin, white) and endogenous Abi protein (green). The clonal border is marked with a yellow dotted line. In wild-type cells (EGFP-negative cells), Abi is enriched at actin-rich protrusions. The arrow shows the direction of the A-P body axis. Bars, 5 µm. The arrowheads highlight tricellular contacts where Abi and F-actin accumulate. The asterisk marks mutant cells with no obvious defects in the formation or alignment of basal actin bundles. (C) Spinning disc time-lapse series of an abi mutant egg chamber stage 6/7 reexpressing a EGFP-tagged Abi rescue transgene. The arrowheads mark the enrichment of Abi at dynamic cell protrusions emerging from tricellular junctions. The arrow indicates the direction of migration. Bars, 5 µm. See also Video 5 A. (D) Spinning disc time-lapse series of an abi mutant egg chamber stage 10 reexpressing an EGFP-tagged Abi rescue transgene. Dynamic finger-like protrusions between follicle cells are marked by Abi-EGFP (arrowheads). Bars, 5 µm. See also Video 5 B.