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    Rac1 and Aurora A regulate MCAK to polarize microtubule growth in migrating endothelial cells.

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    Author
    Braun, A; Dang, K; Buslig, F; Baird, MA; Davidson, MW; Waterman, CM; Myers, KA
    Date
    2014-07-07
    Source Title
    The Journal of Cell Biology
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Myers, Kenneth
    Affiliation
    Medicine and Radiology
    Metadata
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    Document Type
    Journal Article
    Citations
    Braun, A., Dang, K., Buslig, F., Baird, M. A., Davidson, M. W., Waterman, C. M. & Myers, K. A. (2014). Rac1 and Aurora A regulate MCAK to polarize microtubule growth in migrating endothelial cells.. J Cell Biol, 206 (1), pp.97-112. https://doi.org/10.1083/jcb.201401063.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257182
    DOI
    10.1083/jcb.201401063
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4085700
    Abstract
    Endothelial cells (ECs) migrate directionally during angiogenesis and wound healing by polarizing to extracellular cues to guide directional movement. EC polarization is controlled by microtubule (MT) growth dynamics, which are regulated by MT-associated proteins (MAPs) that alter MT stability. Mitotic centromere-associated kinesin (MCAK) is a MAP that promotes MT disassembly within the mitotic spindle, yet its function in regulating MT dynamics to promote EC polarity and migration has not been investigated. We used high-resolution fluorescence microscopy coupled with computational image analysis to elucidate the role of MCAK in regulating MT growth dynamics, morphology, and directional migration of ECs. Our results show that MCAK-mediated depolymerization of MTs is specifically targeted to the trailing edge of polarized wound-edge ECs. Regulation of MCAK function is dependent on Aurora A kinase, which is regionally enhanced by signaling from the small guanosine triphosphatase, Rac1. Thus, a Rac1-Aurora A-MCAK signaling pathway mediates EC polarization and directional migration by promoting regional differences in MT dynamics in the leading and trailing cell edges.

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