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@ARTICLE{Dupraz:141611,
      author       = {Dupraz, Sebastian and Hilton, Brett J and Husch, Andreas
                      and Da Silva Santos, Telma and Coles, Charlotte H and Stern,
                      Sina and Brakebusch, Cord and Bradke, Frank},
      title        = {{R}ho{A} {C}ontrols {A}xon {E}xtension {I}ndependent of
                      {S}pecification in the {D}eveloping {B}rain.},
      journal      = {Current biology},
      volume       = {29},
      number       = {22},
      issn         = {0960-9822},
      address      = {London},
      publisher    = {Current Biology Ltd.},
      reportid     = {DZNE-2020-07935},
      pages        = {3874-3886.e9},
      year         = {2019},
      abstract     = {The specification of an axon and its subsequent outgrowth
                      are key steps during neuronal polarization, a prerequisite
                      to wire the brain. The Rho-guanosine triphosphatase (GTPase)
                      RhoA is believed to be a central player in these processes.
                      However, its physiological role has remained undefined.
                      Here, genetic loss- and gain-of-function experiments
                      combined with time-lapse microscopy, cell culture, and
                      in vivo analysis show that RhoA is not involved in axon
                      specification but confines the initiation of neuronal
                      polarization and axon outgrowth during development.
                      Biochemical analysis and super-resolution microscopy
                      together with molecular and pharmacological manipulations
                      reveal that RhoA restrains axon growth by activating
                      myosin-II-mediated actin arc formation in the growth cone
                      to prevent microtubules from protruding toward the leading
                      edge. Through this mechanism, RhoA regulates the duration of
                      axon growth and pause phases, thus controlling the tightly
                      timed extension of developing axons. Thereby, this work
                      unravels physiologically relevant players coordinating
                      actin-microtubule interactions during axon growth.},
      keywords     = {Actin Cytoskeleton: metabolism / Actins: metabolism /
                      Animals / Axons: metabolism / Axons: physiology / Brain:
                      embryology / Brain: metabolism / Cell Polarity: physiology /
                      Female / Gain of Function Mutation: genetics / Growth Cones:
                      metabolism / Loss of Function Mutation: genetics / Male /
                      Mice / Mice, Inbred C57BL / Mice, Transgenic / Microtubules:
                      metabolism / Myosin Type II: metabolism / Neurogenesis:
                      physiology / Neurons: metabolism / rhoA GTP-Binding Protein:
                      genetics / rhoA GTP-Binding Protein: metabolism / rhoA
                      GTP-Binding Protein: physiology},
      cin          = {AG Bradke},
      ddc          = {570},
      cid          = {I:(DE-2719)1013002},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31679934},
      doi          = {10.1016/j.cub.2019.09.040},
      url          = {https://pub.dzne.de/record/141611},
}