Selective Filopodia Adhesion Ensures Robust Cell Matching in the Drosophila Heart

The ability to form specific cell-cell connections within complex cellular environments is critical for multicellular organisms. However, the underlying mechanisms of cell matching that instruct these connections remain elusive. Here, we explore the dynamic regulation of matching processes utilizing Drosophila cardiogenesis. During embryonic heart formation, cardioblasts (CBs) form precise contacts with their partners after long-range migration. We find that CB matching is highly robust at the boundaries between distinct CB subtypes. Filopodia in these CB subtypes have different binding affinities. We identify the adhesion molecules Fasciclin III (Fas3) and Ten-m as having complementary differential expression in CBs. Altering Fas3 expression influences the CB filopodia selective binding activities and CB matching. In contrast to single knockouts, loss of both Fas3 and Ten-m dramatically impairs CB alignment. We propose that differential expression of adhesion molecules mediates selective filopodia binding, and these molecules work in concert to instruct precise and robust cell matching.