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Article Dans Une Revue Frontiers in Cellular Neuroscience Année : 2018

A Fat-Facets-Dscam1-JNK Pathway Enhances Axonal Growth in Development and after Injury

Marta Koch
  • Fonction : Auteur
Maya Nicolas
  • Fonction : Auteur
Marlen Zschaetzsch
  • Fonction : Auteur
Natalie de Geest
  • Fonction : Auteur
Annelies Claeys
  • Fonction : Auteur
Jiekun Yan
  • Fonction : Auteur
Matthew J Morgan
  • Fonction : Auteur
  • PersonId : 914393
Maria-Luise Erfurth
  • Fonction : Auteur
Matthew Holt
Dietmar Schmucker
  • Fonction : Auteur

Résumé

Injury to the adult central nervous systems (CNS) can result in severe long-term disability because damaged CNS connections fail to regenerate after trauma. Identification of regulators that enhance the intrinsic growth capacity of severed axons is a first step to restore function. Here, we conducted a gain-of-function genetic screen in Drosophila to identify strong inducers of axonal growth after injury. We focus on a novel axis the Down Syndrome Cell Adhesion Molecule (Dscam1), the de-ubiquitinating enzyme Fat Facets (Faf)/Usp9x and the Jun N-Terminal Kinase (JNK) pathway transcription factor Kayak (Kay)/Fos. Genetic and biochemical analyses link these genes in a common signaling pathway whereby Faf stabilizes Dscam1 protein levels, by acting on the 3′-UTR of its mRNA, and Dscam1 acts upstream of the growth-promoting JNK signal. The mammalian homolog of Faf, Usp9x/FAM, shares both the regenerative and Dscam1 stabilizing activities, suggesting a conserved mechanism.

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Neurobiologie
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hal-01718099 , version 1 (27-02-2018)

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Marta Koch, Maya Nicolas, Marlen Zschaetzsch, Natalie de Geest, Annelies Claeys, et al.. A Fat-Facets-Dscam1-JNK Pathway Enhances Axonal Growth in Development and after Injury. Frontiers in Cellular Neuroscience, 2018, 11, pp.416. ⟨10.3389/fncel.2017.00416⟩. ⟨hal-01718099⟩
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