GTPase-activating protein, which acts as a negative regulator for some members of the Ras family (By similarity). Probably decreases their signaling activity by stimulating their intrinsic GTPase activity, thereby lowering the levels of the GTP-bound active form (By similarity). Functions with DE-cadherin (shg) to promote embryonic border cell (BC) migration and adhesion by regulating the distribution of actin protrusions in BCs (PubMed:30763317). Promotes shg-mediated adhesion at the BC interfaces and likely maintains BC cluster adhesion during BC detachment from the follicular epithelium and subsequent BC migration (PubMed:30763317). Also required for restricting the development of actin-rich protrusions to the front of migrating BC clusters thus ensuring unidirectional BC migration (PubMed:30763317). Possibly functions by suppressing Rac1 signaling in non-leading BCs, thus limiting its activity to leading BCs where it initiates localized actin cytoskeleton remodeling to produce the polarized protrusions (PubMed:30763317). In embryos before border cell (BC) delamination and during BC migration (stage 8 and stage 9 egg chambers), colocalizes with E-cad/shg at the cell membranes of BCs and polar cells (PCs), and is enriched at the PC apical membrane. Also colocalizes with shg in the aminoserosa cell contacts and the dorsal most ectodermal cells at the zippering interface. Cytoplasmic levels are higher in PCs compared to BCs. Detected in stage 8 and stage 9 egg chambers (at protein level). RNAi-mediated knockdown in both the border cells (BCs) and follicle cells (FCs), results in the abnormal distribution of F-actin protrusions which extend from the BC cluster. However, the number of actin protrusions is not significantly affected. RNAi-mediated knockdown in the embryonic polar cells (PCs) results in BC dissociation in 63 percent of egg chambers. The name 'raskol' means 'to split' in Russian, and is based upon its role in maintaining cell adhesion in the polar and border cells of embryos.