End-binding proteins EB3 and EB1 link microtubules to ankyrin G in the axon initial segment

DOI Web Site 4 Citations
  • Christophe Leterrier
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and
  • Hélène Vacher
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and
  • Marie-Pierre Fache
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and
  • Stéphanie Angles d'Ortoli
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and
  • Francis Castets
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and
  • Amapola Autillo-Touati
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and
  • Bénédicte Dargent
    Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 641, F-13916 Marseille, France; and

Abstract

<jats:p>The axon initial segment (AIS) plays a key role in maintaining the molecular and functional polarity of the neuron. The relationship between the AIS architecture and the microtubules (MTs) supporting axonal transport is unknown. Here we provide evidence that the MT plus-end-binding (EB) proteins EB1 and EB3 have a role in the AIS in addition to their MT plus-end tracking protein behavior in other neuronal compartments. In mature neurons, EB3 is concentrated and stabilized in the AIS. We identified a direct interaction between EB3/EB1 and the AIS scaffold protein ankyrin G (ankG). In addition, EB3 and EB1 participate in AIS maintenance, and AIS disassembly through ankG knockdown leads to cell-wide up-regulation of EB3 and EB1 comets. Thus, EB3 and EB1 coordinate a molecular and functional interplay between ankG and the AIS MTs that supports the central role of ankG in the maintenance of neuronal polarity.</jats:p>

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