Filopodia (also microspikes) are slender cytoplasmic projections that extend beyond the leading edge of lamellipodia in migrating cells.[1] They contain actin filaments cross-linked into bundles by actin-binding proteins, e.g. fascin and fimbrin.[2] Filopodia form focal adhesions with the substratum, linking it to the cell surface.[3] Many types of migrating cells display filopodia, which are thought to be involved in both sensation of chemotropic cues, and resulting changes in directed locomotion.
Activation of the Rho family of small Ras-related GTPases, particularly cdc42 and their downstream intermediates results in the polymerization of actin fibers by Ena/Vasp homology proteins.[4] Growth factors bind to receptor tyrosine kinases resulting in the polymerization of actin filaments, which, when cross-linked, make up the supporting cytoskeletal elements of filopodia. Rho activity also results in the activation of the phosphorylation of the ezrin-moesin-radixin group promoting the binding of actin filaments to the filopodia membrane.[4]
To close a wound in vertebrates, growth factors stimulate the formation of filopodia in fibroblasts to direct fibroblast migration and wound closure.[5] In developing neurons, filopodia extend from the growth cone at the leading edge. In neurons deprived of filopodia by partial inhibition of actin filaments polymerization, growth cone extension continues as normal but direction of growth is disrupted and highly irregular.[5] In macrophages, filopodia act as phagocytic tentacles and pull bound objects towards the cell for phagocytosis.[6]
Filopodia are also used for movement of bacteria between cells, so as to evade the host immune system. The intracellular bacteria Ehrlichia are transported between cells through the host cell filopodia induced by the pathogen during initial stages of infection.[7]