Fig. 1. Domeless controls border cell migration and interacts with the JAK/STAT pathway. (A) Schematic representation of BCs (in red) during stages 8 to 10. The BC cluster, containing the polar cells (in black), starts to delaminate from the follicle cell layer (in grey) during stage 9 and invades the nurse cell compartment (in blue). At stage 10, BCs reach the anterior of the developing oocyte (in yellow). (B) Wild-type stage 10 egg chamber stained with phalloidin-FITC (green; staining the actin cytoskeleton) and propidium iodide (red; staining the nuclei). Note the round BC cluster at the anterior of the oocyte (arrowhead). (C) Stage 9 egg chamber from an heterozygous dome^PL100/+ female. The BC cluster is not correctly assembled with some cells being left behind (arrowheads). (D,E) Mosaic egg chambers containing dome mutant clones (recognized by the absence of the GFP clonal marker and upregulation of the Fas3 marker (in red; see also Fig. 7). Loss of dome in BC precursors leads to defective, or absence of, BC migration. For comparison, the normal position of the cluster as it would be in a wild-type chamber is represented by a dashed circle. (F,G) Early stage 2-3 dome egg chambers showing incomplete encapsulation (arrowheads, F) or fusion (G). Anti-Dome staining is in red. (H) dome interacts genetically with Stat92E and dpias. Histogram representing the percentage of egg chambers of various genotypes with BC migration phenotypes similar to those shown in C or with defective BCs at stages 9 and 10. (I,J) dome homozygous mutant follicle cells (GFP negative) show a dramatic reduction in nuclear Stat92E (in red). Anterior is to the left.

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