a fat-facets-dscam1-jnk pathway enhances axonal growth in development and after injury

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ID: 215291
2018
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Abstract
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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koch2018frontiersa Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Marta Koch;Marta Koch;Maya Nicolas;Maya Nicolas;Marlen Zschaetzsch;Marlen Zschaetzsch;Natalie de Geest;Natalie de Geest;Annelies Claeys;Annelies Claeys;Jiekun Yan;Jiekun Yan;Matthew J. Morgan;Matthew J. Morgan;Maria-Luise Erfurth;Maria-Luise Erfurth;Matthew Holt;Matthew Holt;Dietmar Schmucker;Dietmar Schmucker;Bassem A. Hassan;Bassem A. Hassan;Bassem A. Hassan
Journal macromolecular bioscience
Year 2018
DOI
10.3389/fncel.2017.00416
URL
http://journal.frontiersin.org/article/10.3389/fncel.2017.00416/full
Keywords
central nervous system neuropsychiatry biological psychiatry post-transcriptional reguylatiopn

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