Cadherins are calcium-dependent cell adhesion proteins (PubMed:7958432). In connecting cells they preferentially interact with themselves in a homophilic manner; cadherins may thus contribute to the sorting of heterogeneous cell types (PubMed:7958432). During oogenesis, integral component of the guidance mechanisms that regulate the directional persistent collective migration of the border cell (BC) cluster through the nurse cells to the oocyte (PubMed:24855950, PubMed:30763317). Functions downstream of the two chemoattractant receptors, Pvr and Egfr, to promote BC adhesion between the leader cells of the migrating cluster and the surrounding nurse cells (PubMed:24855950). This adhesion increases Rac1 signaling in the leading cells, which in turn stabilizes DE-cadherin/DE-cadherin adhesions through the formation of forward-directed protrusions which attach/detach to the surrounding nurse cells in order to pull the cluster through the egg chamber to the oocyte (PubMed:24855950). Within the BC cluster, also promotes adhesion between BCs, and between BCs and polar cells which enables the lead BC to communicate direction to the other cells in the cluster, providing polarity to each individual cell and ensuring collective behavior (PubMed:24855950, PubMed:30763317). May function in cell intercalation in the lateral epidermis during germband extension (PubMed:24681004). Contributes to the determination of body left-right asymmetry by enhancing Myo31DF activity and inhibiting Myo61F activity (PubMed:22491943). Interacts (via cytoplasmic region) with Inx2 (via cytoplasmic loop) (PubMed:15047872). Interacts with Hakai (PubMed:19682089). Interacts with Myo31DF (PubMed:22491943). In stage 8 embryos (before border cell (BC) delimination), and during BC migration, colocalizes with raskol at the cell membranes of BCs and polar cells (PCs), and is enriched at the PC apical membrane. Also colocalizes with raskol in the aminoserosa cell contacts and the dorsal most ectodermal cells at the zippering interface. In early stage 9 and stage 10 oocytes, expressed in border cells, strongly expressed in polar cells and very weakly expressed in the nurse cells (at protein level) (PubMed:24855950). In the embryo, expressed in the leading edge cells of the dorsal epidermis (at protein level) (PubMed:16831834, PubMed:30763317). Stage 10 embryos exhibit intense expression in epithelial cells (PubMed:7958432). Stage 14 embryos show expression in the hindgut (at the apical poles of cell-cell boundaries), at the apical junctions of tracheal cells and in the dorsal longitudinal trunk (PubMed:7958432). In stage 16 embryos the glial midline cells of the central nervous system show strong expression (PubMed:7958432). Three calcium ions are usually bound at the interface of each cadherin domain and rigidify the connections, imparting a strong curvature to the full-length ectodomain. N-glycosylation is important for biosynthesis and function. RNAi-mediated knockdown in segment A8 of the male genital disk causes loss of the normal dextral rotation of the genital plate and results in a phenotype with no rotation (PubMed:22491943). During oocyte border cell migration, RNAi-mediated knockdown in either the border cells (BC) or in the surrounding nurse cells results in various BC migration defects such as BC deviating from their migration path or failing to sustain the directed, posterior movement (PubMed:30763317, PubMed:24855950). RNAi-mediated knockdown in the outer migratory BC disrupts distribution of Rac1 in the BC cluster but does not affect motility and cells remain clustered (PubMed:24855950). RNAi-mediated knockdown in oocyte polar cells (PCs) results in BC cluster dissociation in 80 percent of egg chambers (PubMed:30763317). Overexpression in segment A8 of the male genital disk has no effect on the normal dextral rotation of the genital plate.