Filopodia

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The filopodia (also microspikes) are slender cytoplasmic projections, similar to lamellipodia, which extend from the leading edge of migrating cells.[1] They contain actin filaments cross-linked into bundles by actin-binding proteins, e.g. fimbrin.[2] Filopodia form focal adhesions with the substratum, linking it to the cell surface [3]. A cell migrates along a surface by extending filopodia at the leading edge. The filopodia attach to the substratum further down the migratory pathway, then contraction of stress fibres retracts the rear of the cell to move the cell forwards.

Activation of the Rho family of small Ras-related GTPases, particularly cdc42 and their downstream intermediates results in the construction of actin fibers[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 division and close the wound.[5] In developing neurons, filopodia extend from the growth cone at the leading edge. In neurons deprived of filopodia by the removal of actin filaments, 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]

References

  1. ^ Mattila PK, Lappalainen P (June 2008). "Filopodia: molecular architecture and cellular functions". Nat. Rev. Mol. Cell Biol. 9 (6): 446–54. doi:10.1038/nrm2406. PMID 18464790. 
  2. ^ Hanein D, Matsudaira P, DeRosier DJ (October 1997). "Evidence for a conformational change in actin induced by fimbrin (N375) binding". J. Cell Biol. 139 (2): 387–96. doi:10.1083/jcb.139.2.387. PMID 9334343. http://www.jcb.org/cgi/pmidlookup?view=long&pmid=9334343. 
  3. ^ Molecular Cell Biology Fifth Edition Lodish, Berk, Matsudaira, Kaiser, Krieger, Scott, Zipursky, Darnell. pg. 821, 823 2004 by W.H. Freeman and Company.
  4. ^ a b Ohta Y, Suzuki N, Nakamura S, Hartwig JH, Stossel TP (March 1999). "The small GTPase RalA targets filamin to induce filopodia". Proc. Natl. Acad. Sci. U.S.A. 96 (5): 2122–8. doi:10.1073/pnas.96.5.2122. PMID 10051605. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=10051605. 
  5. ^ a b Bentley D, Toroian-Raymond A (1986). "Disoriented pathfinding by pioneer neurone growth cones deprived of filopodia by cytochalasin treatment". Nature 323 (6090): 712–5. doi:10.1038/323712a0. PMID 3773996. 
  6. ^ Kress H, Stelzer EH, Holzer D, Buss F, Griffiths G, Rohrbach A (2007). "Filopodia act as phagocytic tentacles and pull with discrete steps and a load-dependent velocity". Proc. Natl. Acad. Sci. U.S.A. 104 (28): 11633-11638. doi:10.1073/pnas.0702449104. PMID 17620618. http://www.pnas.org/content/104/28/11633.abstract. 
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