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    Coordination by Cdc42 of actin, contractility, and adhesion for melanoblast movement in mouse skin

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    Swaminathan_Current_Biology.pdf (12.13Mb)
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    Publication date
    2017-03
    Author
    Woodham, E.F.
    Paul, N.R.
    Tyrrell, B.
    Spence, H.J.
    Swaminathan, Karthic
    Scribner, M.R.
    Giampazolias, E.
    Hedley, A.
    Clark, W.
    Kage, F.
    Marston, D.J.
    Hahn, K.M.
    Tait, S.W.G.
    Larue, L.
    Brakebusch, C.H.
    Insall, R.H.
    Machesky, L.M.
    Show allShow less
    Keyword
    Rho GTPases
    Migration
    Actin cytoskeleton
    Cell motility
    Melanocyte
    Myosin
    Actin
    Adhesion
    Integrin
    Cdc42
    Rights
    © 2017 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
    Peer-Reviewed
    Yes
    
    Metadata
    Show full item record
    Abstract
    The individual molecular pathways downstream of Cdc42, Rac, and Rho GTPases are well documented, but we know surprisingly little about how these pathways are coordinated when cells move in a complex environment in vivo. In the developing embryo, melanoblasts originating from the neural crest must traverse the dermis to reach the epidermis of the skin and hair follicles. We previously established that Rac1 signals via Scar/WAVE and Arp2/3 to effect pseudopod extension and migration of melanoblasts in skin. Here we show that RhoA is redundant in the melanocyte lineage but that Cdc42 coordinates multiple motility systems independent of Rac1. Similar to Rac1 knockouts, Cdc42 null mice displayed a severe loss of pigmentation, and melanoblasts showed cell-cycle progression, migration, and cytokinesis defects. However, unlike Rac1 knockouts, Cdc42 null melanoblasts were elongated and displayed large, bulky pseudopods with dynamic actin bursts. Despite assuming an elongated shape usually associated with fast mesenchymal motility, Cdc42 knockout melanoblasts migrated slowly and inefficiently in the epidermis, with nearly static pseudopods. Although much of the basic actin machinery was intact, Cdc42 null cells lacked the ability to polarize their Golgi and coordinate motility systems for efficient movement. Loss of Cdc42 de-coupled three main systems: actin assembly via the formin FMNL2 and Arp2/3, active myosin-II localization, and integrin-based adhesion dynamics.
    URI
    http://hdl.handle.net/10454/17713
    Version
    Published version
    Citation
    Woodham EF, Paul NR, Tyrrell B et al (2017) Coordination by Cdc42 of actin, contractility, and adhesion for melanoblast movement in mouse skin. Current Biology. 27(5): 624-637.
    Link to publisher’s version
    https://doi.org/10.1016/j.cub.2017.01.033
    Type
    Article
    Collections
    Life Sciences Publications

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