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The small GTPase RalA targets filamin to induce filopodia.

The Ras-related small GTPases Rac, Rho, Cdc42, and RalA bind filamin, an actin filament-crosslinking protein that also links membrane and other intracellular proteins to actin. Of these GTPases only RalA binds filamin in a GTP-specific manner, and GTP-RalA elicits actin-rich filopods on surfaces of Swiss 3T3 cells and recruits filamin into the filopodial cytoskeleton. Either a dominant negative RalA construct or the RalA-binding domain of filamin 1 specifically block Cdc42-induced filopod formation, but a Cdc42 inhibitor does not impair RalA's effects, which, unlike Cdc42, are Rac independent. RalA does not generate filopodia in filamin-deficient human melanoma cells, whereas transfection of filamin 1 restores the functional response. RalA therefore is a downstream intermediate in Cdc42- mediated filopod production and uses filamin in this pathway.[1]

References

  1. The small GTPase RalA targets filamin to induce filopodia. Ohta, Y., Suzuki, N., Nakamura, S., Hartwig, J.H., Stossel, T.P. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
 
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