ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Injury-dependent Müller glia and ganglion cell reprogramming during tissue regeneration requires Apobec2a and Apobec2b.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Zebrafish optic nerve injury results in systemic retinal ganglion cell dedifferentiation.PLoS genetics · 2025Article
- Article
- APOBEC2 safeguards skeletal muscle cell fate through binding chromatin and regulating transcription of non-muscle genes during myoblast differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Unlocking the potential for optic nerve regeneration over long distances: a multi-therapeutic intervention.Frontiers in neurology · 2024Review
- Intraocular Axon Regeneration in a Model of Penetrating Eye Injury.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2023Article
- Optic nerve diseases and regeneration: How far are we from the promised land?Clinical & experimental ophthalmology · 2023Review
- Direct neuronal reprogramming by temporal identity factors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Generating Widespread and Scalable Retinal Lesions in Adult Zebrafish by Intraocular Injection of Ouabain.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Epigenetic mechanisms of Müller glial reprogramming mediating retinal regeneration.Frontiers in cell and developmental biology · 2023Review
- Assessing Rewiring of the Retinal Circuitry by Electroretinogram (ERG) After Inner Retinal Lesion in Adult Zebrafish.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Regenerative neurogenesis: the integration of developmental, physiological and immune signals.Development (Cambridge, England) · 2022Article
- Article
- In vivo glial trans-differentiation for neuronal replacement and functional recovery in central nervous system.The FEBS journal · 2021Review
- Müller Glia-Mediated Retinal Regeneration.Molecular neurobiology · 2021Review
- Advances in Regeneration of Retinal Ganglion Cells and Optic Nerves.International journal of molecular sciences · 2021Review
- Reprogramming Müller Glia to Regenerate Retinal Neurons.Annual review of vision science · 2020Review
- DNA demethylation is a driver for chick retina regeneration.Epigenetics · 2020Article
- Epigenetics in neuronal regeneration.Seminars in cell & developmental biology · 2020Review
- miRNAs and Müller Glia Reprogramming During Retina Regeneration.Frontiers in cell and developmental biology · 2020Review
- Role ofGenes · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Unlike mammals, adult zebrafish are able to regenerate multiple tissues including those of the CNS. In the zebrafish retina, injury stimulates Müller glia dedifferentiation into a multipotent retinal progenitor that is capable of regenerating all lost cell types. This dedifferentiation is driven by the reactivation of gene expression programs that share many characteristics with those that operate during early development. Although the mechanisms underlying the reactivation of these programs remain unknown, it is likely that changes in DNA methylation play a significant role. To begin investigating whether DNA demethylation may contribute to retina regeneration, we characterized the expression of genes associated with DNA demethylation in the uninjured and injured retina. We found that two cytidine deaminases (apobec2a and apobec2b) were expressed basally in the uninjured retina and that they were induced in proliferating, dedifferentiated Müller glia. The maximal induction of apobec2b required Ascl1a, but was independent of Lin28, and therefore defines an independent signaling pathway stemming from Ascl1a. Strikingly, when Apobec2a or Apobec2b was knocked down by antisense morpholino oligonucleotides, the proliferative response of Müller glia following injury was significantly reduced and injury-dependent induction of ascl1a and its target genes were inhibited, suggesting the presence of a regulatory feedback loop between Apobec proteins and ascl1a. Finally, Ascl1a, Apobec2a and Apobec2b were found to be essential for optic nerve regeneration. These data identify an essential role for Apobec proteins during retina and optic nerve regeneration and suggest DNA demethylation may underlie the reprogramming of cells to mount a regenerative response.
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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.