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

Frontiers in Cellular Neuroscience
Marta KochBassem A Hassan

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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Citations

Jan 31, 2018·Frontiers in Molecular Neuroscience·Wilson Pak-Kin LouAna Martin-Villalba
Mar 19, 2019·Annual Review of Neuroscience·Claire E Richardson, Kang Shen

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Methods Mentioned

BETA
de-ubiquitination
ubiquitination
Electrophoresis

Software Mentioned

Zeiss Zen
IMAGE
Image J
ImageJ

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The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
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