| Autor: |
Mellentine SQ; Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA 52242., Ramsey AS; Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA 52242., Li J; Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA 52242., Brown HN; Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA 52242., Tootle TL; Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA 52242. |
| Abstrakt: |
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 Drosophila border cell migration as a model to uncover the cell-specific roles of two PGs in collective migration. Prior work shows PG signaling is required for on-time migration and cluster cohesion. We find that the PGE 2 synthase cPGES is required in the substrate, while the PGF 2α 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 regulates border cell migration 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. Together these data reveal that two PGs, PGE 2 and PGF 2α , 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. |
