World Library  
Flag as Inappropriate
Email this Article

Filopodia

Article Id: WHEBN0004102360
Reproduction Date:

Title: Filopodia  
Author: World Heritage Encyclopedia
Language: English
Subject: Ena/Vasp homology proteins, Neuronal self-avoidance, Paracytophagy, SRGAP2, Pseudopodia
Collection:
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Filopodia

This electron micrograph shows exaggerated filopodia with club-like shape induced by formin mDia2 in cultured cells. These filopodia are filled with bundled actin filaments which were born in and converged from the lamellipodial network.

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 activation by phosphorylation of ezrin-moesin-radixin family proteins that link actin filaments to the filopodia membrane.[4]

Filopodia have roles in sensing, migration and cell-cell interaction.[1] 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] Filopodia-like projections have also been linked to dendrite creation when new synapses are formed in the brain.[6][7] In macrophages, filopodia act as phagocytic tentacles and pull bound objects towards the cell for phagocytosis.[8]

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.[9] Viruses were shown to be transported along filopodia toward the cell body, leading to cell infection.[10] Directed transport of receptor-bound epidermal growth factor (EGF) along filopodia has also been described, supporting the proposed sensing function of filopodia.[11]

References

  1. ^ a b Mattila PK, Lappalainen P (June 2008). "Filopodia: molecular architecture and cellular functions". Nat. Rev. Mol. Cell Biol. 9 (6): 446–54.  
  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.  
  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.  
  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.  
  6. ^ Beardsley, John (June 1999). "Getting Wired". Scientific American. 
  7. ^ Maletic-Savatic, M.; Malinow R. (June 1999). "Rapid Dendritic Morphogenesis in CA1 Hippocampal Dendrites Induced by Synaptic Activity". Science.  
  8. ^ 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.  
  9. ^ Thomas S, Popov VL, Walker DH (2010) Exit Mechanisms of the Intracellular Bacterium Ehrlichia" PLoS ONE 5(12) e15775. http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0015775
  10. ^ Lehmann MJ, Sherer NM, Marks CB, Pypaert M, Mothes W (2005). "Actin- and myosin-driven movement of viruses along filopodia precedes their entry into cells.". J Cell Biol 170 (2): 317–325.  
  11. ^ Lidke, DS; Lidke, KA; Rieger, B; Jovin, TM; Arndt-Jovin, DJ (Aug 15, 2005). "Reaching out for signals: filopodia sense EGF and respond by directed retrograde transport of activated receptors.". The Journal of Cell Biology 170 (4): 619–26.  

External links

  • MBInfo - Filopodia
  • MBInfo - Filopodia Assembly
  • [1]
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.