ArticleFrontiers in cellular neuroscience2017
A Fat-Facets-Dscam1-JNK Pathway Enhances Axonal Growth in Development and after Injury.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The adiponectin-depression nexus: a brief review of mechanisms and therapeutic opportunities.Metabolic brain disease · 2026Review
- The deubiquitylating enzyme Fat facets promotes Fat signalling and restricts tissue growth.Nature communications · 2025Article
- JNK signaling in pioneer neurons organizes ventral nerve cord architecture in Drosophila embryos.Nature communications · 2023Article
- Insights into nervous system repair from the fruit fly.Neuronal signaling · 2022Review
- Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid βBMC neuroscience · 2021Article
- Regulation of Adult CNS Axonal Regeneration by the Post-transcriptional Regulator Cpeb1.Frontiers in molecular neuroscience · 2017Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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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