Journal
DEVELOPMENTAL CELL
Volume 12, Issue 4, Pages 603-614Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2007.03.005
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Funding
- NIGMS NIH HHS [R01 GM034933, R37 GM028007-28, R37 GM028007, R01 GM034933-21] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM034933, R37GM028007] Funding Source: NIH RePORTER
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Directed cell migration involves signaling events that lead to local accumulation of PI(3,4,5)P-3, but additional pathways act in parallel. A genetic screen in Dictyostelium discoideum, to identify redundant pathways revealed a gene with homology to patatin-like phospholipase A(2). Loss of this gene did not alter PI(3,4,5)P-3 regulation, but chemotaxis became sensitive to reductions in PI3K activity. Likewise, cells deficient in PI3K activity were more sensitive to inhibition of PLA(2) activity. Deletion of the PLA(2) homolog and two PI3Ks caused a strong defect in chemotaxis and a reduction in receptor-mediated actin polymerization. In wild-type cells, chemoattractants stimulated a rapid burst in an arachidonic acid derivative. This response was absent in cells lacking the PLA(2) homolog, and exogenous arachidonic acid reduced their dependence on PI3K signaling. We propose that PLA(2) and PI3K signaling act in concert to mediate chemotaxis, and metabolites of PLA(2) may be important mediators of the response.
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