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      SAD kinases sculpt axonal arbors of sensory neurons through long- and short-term responses to neurotrophin signals.

      1 , ,
      Neuron
      Elsevier BV

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          Abstract

          Extrinsic cues activate intrinsic signaling mechanisms to pattern neuronal shape and connectivity. We showed previously that three cytoplasmic Ser/Thr kinases, LKB1, SAD-A, and SAD-B, control early axon-dendrite polarization in forebrain neurons. Here, we assess their role in other neuronal types. We found that all three kinases are dispensable for axon formation outside of the cortex but that SAD kinases are required for formation of central axonal arbors by subsets of sensory neurons. The requirement for SAD kinases is most prominent in NT-3 dependent neurons. SAD kinases transduce NT-3 signals in two ways through distinct pathways. First, sustained NT-3/TrkC signaling increases SAD protein levels. Second, short-duration NT-3/TrkC signals transiently activate SADs by inducing dephosphorylation of C-terminal domains, thereby allowing activating phosphorylation of the kinase domain. We propose that SAD kinases integrate long- and short-duration signals from extrinsic cues to sculpt axon arbors within the CNS.

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          Author and article information

          Journal
          Neuron
          Neuron
          Elsevier BV
          1097-4199
          0896-6273
          Jul 10 2013
          : 79
          : 1
          Affiliations
          [1 ] Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.
          Article
          S0896-6273(13)00437-6 NIHMS483041
          10.1016/j.neuron.2013.05.017
          3725037
          23790753
          daf79ffb-2507-4da5-a78e-bf49fa8d6ac1
          History

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