Specific prostaglandins are produced in the migratory cells and the surrounding substrate to promote border cell migration.

A key regulator of collective cell migration is prostaglandin (PG) signaling. However, it remains largely unclear whether PGs act within the migratory cells or their microenvironment to promote migration. Here we use border cell migration as a model to uncover the cell-specific roles of two PGs in collective migration. The border cells undergo a collective and invasive migration between the nurse cells; thus, the nurse cells are the substrate and microenvironment for the border cells. Prior work found PG signaling is required for on-time border cell migration and cluster cohesion. Confocal microscopy and quantitative image analyses of available mutant alleles and RNAi lines were used to define the roles of the PGE and PGF synthases in border cell migration. We find that the PGE synthase cPGES is required in the substrate, while the PGF synthase Akr1B is required in the border cells for on-time migration. Akr1B acts in both the border cells and their substrate to regulate cluster cohesion. One means by which Akr1B may regulate border cell migration and/or cluster cohesion is by promoting integrin-based adhesions. Additionally, Akr1B limits myosin activity, and thereby cellular stiffness, in the border cells, whereas cPGES limits myosin activity in both the border cells and their substrate. Decreasing myosin activity overcomes the migration delays in both and mutants, indicating the changes in cellular stiffness contribute to the migration defects. Together these data reveal that two PGs, PGE and PGF, produced in different locations, play key roles in promoting border cell migration. These PGs likely have similar migratory versus microenvironment roles in other collective cell migrations.