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Mol. Cell. Biol. doi:10.1128/MCB.00150-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Elongation factor eEF1A2 cooperates with phosphatidylinositol-4 kinaseIII to stimulate filopodia production through increased PI(4,5)P₂ generation

Department of Biochemistry, Microbiology, & Immunology, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, Canada K1H 8M5

^* To whom correspondence should be addressed. Email: jlee{at}uottawa.ca.

	Abstract

eEF1A2 (eukaryotic elongation factor 1 alpha 2) is a transforming gene highly expressed in human tumors of the ovary, lung and breast (2, 24, 25, 40). eEF1A2 also stimulates actin remodeling and its expression is sufficient to induce the formation of filopodia, long cellular processes composed of bundles of parallel actin filaments (1). Here, we find that eEF1A2 stimulates filopodia formation by increasing the cellular abundance of cytosolic and plasma membrane-bound phosphatidylinositol-4,5 bisphosphate (PI(4,5)P₂). We have previously reported that the eEF1A2 protein binds and activates phosphatidylinositol-4 kinase III beta (PI4KIII) (21) and we find that eEF1A2-dependent PI(4,5)P₂ production and filopodia generation requires PI4KIII. Furthermore, PI4KIII is itself capable of activating both PI(4,5)P₂ production and filopodia creation. We propose a model for filopodia extrusion where eEF1A2 activates PI4KIII and activated PI4KIII stimulates PI(4,5)P₂ and filopodia production by increasing PI4P abundance. Our work suggests an important role for both eEF1A2 and PI4KIII in the control of PI(4,5)P₂ signaling and actin remodeling.