Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 23, Issue 23, Pages 4567-4578Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E12-05-0417
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Funding
- National Institutes of Health [T32GM067795, UL1RR024979]
- American Cancer Society [IRG-77-004-34]
- Molecular and Cellular Biology Graduate Program
- National Science Foundation [MCB-1158527]
- Clinical and Translational Science Awards program
- National Center for Advancing Translational Sciences, National Institutes of Health [UL1RR024979]
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [1158527] Funding Source: National Science Foundation
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Although prostaglandins (PGs)-lipid signals produced downstream of cyclooxygenase (COX) enzymes-regulate actin cytoskeletal dynamics, their mechanisms of action are unknown. We previously established Drosophila oogenesis, in particular nurse cell dumping, as a new model to determine how PGs regulate actin remodeling. PGs, and thus the Drosophila COX-like enzyme Pxt, are required for both the parallel actin filament bundle formation and the cortical actin strengthening required for dumping. Here we provide the first link between Fascin (Drosophila Singed, Sn), an actin-bundling protein, and PGs. Loss of either pxt or fascin results in similar actin defects. Fascin interacts, both pharmacologically and genetically, with PGs, as reduced Fascin levels enhance the effects of COX inhibition and synergize with reduced Pxt levels to cause both parallel bundle and cortical actin defects. Conversely, overexpression of Fascin in the germline suppresses the effects of COX inhibition and genetic loss of Pxt. These data lead to the conclusion that PGs regulate Fascin to control actin remodeling. This novel interaction has implications beyond Drosophila, as both PGs and Fascin-1, in mammalian systems, contribute to cancer cell migration and invasion.
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