ArticleThe Journal of cell biology2016
Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki.
Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed.
- Article
- A neurotrophin functioning with a Toll regulates structural plasticity in a dopaminergic circuit.eLife · 2024Article
- The use of induced pluripotent stem cells as a platform for the study of depression.Frontiers in psychiatry · 2024Review
- Regulation of morphogen pathways by a Drosophila chondroitin sulfate proteoglycan Windpipe.Journal of cell science · 2023Article
- Insights into nervous system repair from the fruit fly.Neuronal signaling · 2022Review
- A novel injury paradigm in the central nervous system of adult Drosophila: molecular, cellular and functional aspects.Disease models & mechanisms · 2021Article
- Regenerative neurogenic response from glia requires insulin-driven neuron-glia communication.eLife · 2021Article
- Neural Tissue Homeostasis and Repair Is Regulated via CS and DS Proteoglycan Motifs.Frontiers in cell and developmental biology · 2021Review
- Review
- Functional analysis of glycosylation using Drosophila melanogaster.Glycoconjugate journal · 2020Review
- Lineage-guided Notch-dependent gliogenesis byDevelopment (Cambridge, England) · 2018Article
- Go and stop signals for glial regeneration.Current opinion in neurobiology · 2017Review
- GlialNeural regeneration research · 2017Review
- Chondroitin sulfate in invertebrate development.Proteoglycan researchArticle
- Latent effects of early-life methylmercury exposure on motor function in Drosophila.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Neuron glia antigen 2 (NG2)-positive glia are repair cells that proliferate upon central nervous system (CNS) damage, promoting functional recovery. However, repair is limited because of the failure of the newly produced glial cells to differentiate. It is a key goal to discover how to regulate NG2 to enable glial proliferation and differentiation conducive to repair. Drosophila has an NG2 homologue called kon-tiki (kon), of unknown CNS function. We show that kon promotes repair and identify the underlying mechanism. Crush injury up-regulates kon expression downstream of Notch. Kon in turn induces glial proliferation and initiates glial differentiation by activating glial genes and prospero (pros). Two negative feedback loops with Notch and Pros allow Kon to drive the homeostatic regulation required for repair. By modulating Kon levels in glia, we could prevent or promote CNS repair. Thus, the functional links between Kon, Notch, and Pros are essential for, and can drive, repair. Analogous mechanisms could promote CNS repair in mammals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.