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Keywords

  • Pleckstrin homology containing family member 5 (Plekhg5) (1)
  • autophagy (1)
  • motoneuron disease (1)
  • regulation (1)
  • synaptic vesicles (1)

Author

  • Binotti, Beyenech (1)
  • Blum, Robert (1)
  • Damme, Markus (1)
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  • Füchtbauer, Ernst-Martin (1)
  • Heimann, Peter (1)
  • Horowitz, Arie (1)
  • Jablonka, Sibylle (1)
  • Jahn, Reinhard (1)
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  • Institut für Klinische Neurobiologie (1)
  • Neurologische Klinik und Poliklinik (1)

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Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease (2017)
Lüningschrör, Patrick ; Binotti, Beyenech ; Dombert, Benjamin ; Heimann, Peter ; Perez-Lara, Angel ; Slotta, Carsten ; Thau-Habermann, Nadine ; von Collenberg, Cora R. ; Karl, Franziska ; Damme, Markus ; Horowitz, Arie ; Maystadt, Isabelle ; Füchtbauer, Annette ; Füchtbauer, Ernst-Martin ; Jablonka, Sibylle ; Blum, Robert ; Üçeyler, Nurcan ; Petri, Susanne ; Kaltschmidt, Barbara ; Jahn, Reinhard ; Kaltschmidt, Christian ; Sendtner, Michael
Autophagy-mediated degradation of synaptic components maintains synaptic homeostasis but also constitutes a mechanism of neurodegeneration. It is unclear how autophagy of synaptic vesicles and components of presynaptic active zones is regulated. Here, we show that Pleckstrin homology containing family member 5 (Plekhg5) modulates autophagy of synaptic vesicles in axon terminals of motoneurons via its function as a guanine exchange factor for Rab26, a small GTPase that specifically directs synaptic vesicles to preautophagosomal structures. Plekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degeneration of axon terminals. Plekhg5-depleted cultured motoneurons show defective axon growth and impaired autophagy of synaptic vesicles, which can be rescued by constitutively active Rab26. These findings define a mechanism for regulating autophagy in neurons that specifically targets synaptic vesicles. Disruption of this mechanism may contribute to the pathophysiology of several forms of motoneuron disease.
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