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. Author manuscript; available in PMC: 2009 Apr 21.
Published in final edited form as: J Cell Sci. 2008 Mar 1;121(Pt 5):551–559. doi: 10.1242/jcs.023333

Fig. 1.

Fig. 1

PtdIns(3,4,5)P3 (PIP3) controls cell motility. Basic cell motility is regulated by a Ras–PI3K–PtdIns(3,4,5)P3–F-actin circuit. During chemotaxis, this circuit becomes restricted to the leading edge, allowing directed movement. Several downstream effectors of PtdIns(3,4,5)P3, such as RacGEFs and Akt, activate F-actin polymerization and myosin assembly (see text for details). Positive-feedback loops (red arrows) allow signal amplification, enhanced actin polymerization at the leading edge and the production of pseudopodia. In addition, Ras effectors, such as TORC2 (target of rapamycin complex 2), regulate the actin cytoskeleton and myosin assembly independently of PI3K and PtdIns(3,4,5)P3 (Lee et al., 2005). TORC2 functions, in part, by phosphorylating Akt in the C-terminal hydrophobic domain (Bhaskar and Hay, 2007). In Dictyostelium, Akt is thus regulated by two Ras-mediated pathways, PI3K and TORC2 (Lee et al., 2005).