Collective cell migration is an essential process for embryonic development, wound healing, and cancer metastasis. One mechanism known to promote cell migration is prostaglandin (PG) signaling. PGs, like PGF2α, are small lipid molecules synthesized by cyclooxygenase (COX) enzymes and PG-specific synthases. PGs are secreted from the source cell and bind to a specific set of G-protein coupled receptors (GPCRs) on a local target cell. Each receptor binding initiates downstream signaling events, leading to various biological processes regulated by PG signaling. To investigate the cell-specific roles of PGF2α in promoting cell migration, we leverage the vast genetic toolkit available in Drosophila melanogaster and the established model of in vivo, invasive, collective cell migration—border cell migration—in this species. We have seen that a global knockout or a somatic cell-specific knockdown of the PGF2α synthase, Akr1B, in the Drosophila ovum causes significant border cell migration delay. We are currently investigating the PGF2α signaling pathway by identifying the PGF2α receptor and its coupled G-protein to understand how the PGF2α signaling pathway promotes collective cell migration.

Publications

Mellentine, S.Q., Brown, H.N., Ramsey, A.S., Li, J., Tootle, T.L. (2024) Specific prostaglandins are produced in the migratory cells and the surrounding substrate to promote Drosophila border cell migration. Front. Cell Dev. Biol., 11. 10.3389/fcell.2023.1257751 PMCID: PMC10327004

Honors and Awards

Genetics T-32 Pre-doctoral Training Grant (2024 - 2025)

Genetics T-32 Pre-doctoral Training Grant (2023 - 2024)