ArticleScientific reports2020
Developmental changes in the accessible chromatin, transcriptome and Ascl1-binding correlate with the loss in Müller Glial regenerative potential.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 39 citations in OpenAlex.
- Ascl1 Represses Müller Glial and Promotes Rod Photoreceptor Fate Through Repressing Notch Signaling in Late Retinal Progenitor Cells.Investigative ophthalmology & visual science · 2026Article
- Global epigenetic immunohistochemical markers reveal developmental connections of distinct cell types during fetal development.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026Article
- Oxidative Stress Signaling and Regenerative Responses in a Larval Zebrafish Model of Retinal Light Damage.Antioxidants (Basel, Switzerland) · 2026Article
- Electrical stimulation combined with p27Kip1 inactivation drives proliferative neurogenic reprogramming of Mueller glia in the adult mouse retina.bioRxiv : the preprint server for biology · 2026Article
- Decoding cell-class specific roles of non-coding variants in human retina.Scientific reports · 2025Article
- Integrative snRNA-seq, molecular docking and dynamics simulations identifies Lasmiditan as drug candidate for Alzheimer's disease.Clinical and translational medicine · 2025Article
- Single-cell transcriptome of retinal myeloid cells in response to transplantation of human neurons reveals reversibility of microglial activation.bioRxiv : the preprint server for biology · 2025Article
- Investigating Müller glia reprogramming in mice: a retrospective of the last decade, and a look to the future.Neural regeneration research · 2025Article
- Stimulating the regenerative capacity of the human retina with proneural transcription factors in 3D cultures.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- An alpha7 nicotinic acetylcholine receptor agonist induces retinal neurogenesis and restores electrophysiological function following blast-induced ocular trauma in adult mice.Frontiers in neuroscience · 2025Article
- Experimental Framework for Assessing Mouse Retinal Regeneration Through Single-Cell RNA-Sequencing.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- Monocyte Invasion into the Retina Restricts the Regeneration of Neurons from Müller Glia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Single-Cell Multiomics Profiling Reveals Heterogeneity of Müller Cells in the Oxygen-Induced Retinopathy Model.Investigative ophthalmology & visual science · 2024Article
- A large-scale CRISPR screen reveals context-specific genetic regulation of retinal ganglion cell regeneration.Development (Cambridge, England) · 2024Article
- ASCL1 induces neurogenesis in human Müller glia.Stem cell reports · 2023Article
- Chromatin access regulates the formation of Müller glia-derived progenitor cells in the retina.Glia · 2023Article
- Transcriptomics of CD29Scientific reports · 2023Article
- Somatic Cell Reprogramming for Nervous System Diseases: Techniques, Mechanisms, Potential Applications, and Challenges.Brain sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Diseases and damage to the retina lead to losses in retinal neurons and eventual visual impairment. Although the mammalian retina has no inherent regenerative capabilities, fish have robust regeneration from Müller glia (MG). Recently, we have shown that driving expression of Ascl1 in adult mouse MG stimulates neural regeneration. The regeneration observed in the mouse is limited in the variety of neurons that can be derived from MG; Ascl1-expressing MG primarily generate bipolar cells. To better understand the limits of MG-based regeneration in mouse retinas, we used ATAC- and RNA-seq to compare newborn progenitors, immature MG (P8-P12), and mature MG. Our analysis demonstrated developmental differences in gene expression and accessible chromatin between progenitors and MG, primarily in neurogenic genes. Overexpression of Ascl1 is more effective in reprogramming immature MG, than mature MG, consistent with a more progenitor-like epigenetic landscape in the former. We also used ASCL1 ChIPseq to compare the differences in ASCL1 binding in progenitors and reprogrammed MG. We find that bipolar-specific accessible regions are more frequently linked to bHLH motifs and ASCL1 binding. Overall, our analysis indicates a loss of neurogenic gene expression and motif accessibility during glial maturation that may prevent efficient reprogramming.
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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.