Microtubule growth activates Rac1 to promote lamellipodial protrusion in fibroblasts.

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  • Additional Information
    • Source:
      Publisher: Macmillan Magazines Ltd Country of Publication: England NLM ID: 100890575 Publication Model: Print Cited Medium: Print ISSN: 1465-7392 (Print) Linking ISSN: 14657392 NLM ISO Abbreviation: Nat Cell Biol Subsets: MEDLINE
    • Publication Information:
      Original Publication: London : Macmillan Magazines Ltd., [1999-
    • Subject Terms:
      Microtubules/*physiology ; rac1 GTP-Binding Protein/*metabolism; 3T3 Cells/drug effects ; 3T3 Cells/physiology ; 3T3 Cells/ultrastructure ; Actins/metabolism ; Animals ; Cell Movement/physiology ; Kinetics ; Mice ; Microtubules/drug effects ; Microtubules/ultrastructure ; Nocodazole/pharmacology ; Paclitaxel/pharmacology
    • Abstract:
      Microtubules are involved in actin-based protrusion at the leading-edge lamellipodia of migrating fibroblasts. Here we show that the growth of microtubules induced in fibroblasts by removal of the microtubule destabilizer nocodazole activates Rac1 GTPase, leading to the polymerization of actin in lamellipodial protrusions. Lamellipodial protrusions are also activated by the rapid growth of a disorganized array of very short microtubules induced by the microtubule-stabilizing drug taxol. Thus, neither microtubule shortening nor long-range microtubule-based intracellular transport is required for activating protrusion. We suggest that the growth phase of microtubule dynamic instability at leading-edge lamellipodia locally activates Rac1 to drive actin polymerization and lamellipodial protrusion required for cell migration.
    • Comments:
      Comment in: Nat Cell Biol. 1999 May;1(1):E12. (PMID: 10559874)
    • Accession Number:
      0 (Actins)
      EC 3.6.5.2 (rac1 GTP-Binding Protein)
      P88XT4IS4D (Paclitaxel)
      SH1WY3R615 (Nocodazole)
    • Publication Date:
      Date Created: 19991113 Date Completed: 19991207 Latest Revision: 20160407
    • Publication Date:
      20221213
    • Accession Number:
      10.1038/9018
    • Accession Number:
      10559863