ArticleDevelopment (Cambridge, England)2011
Ascl1 expression defines a subpopulation of lineage-restricted progenitors in the mammalian retina.
Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 3 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
- In vivo and ex vivo evaluation of the responses of rat Müller glia after injury.Scientific reports · 2026Article
- Roles of sonic hedgehog signaling in retinal patterning and neurogenesis during mammalian eye development.Development (Cambridge, England) · 2026Article
- Disease-associated microRNA, miR-9-2, regulates timing of retinal progenitor cell competence and maintenance of Müller glial identity.bioRxiv : the preprint server for biology · 2026Article
- Article
- Lineage tracing reveals photoreceptor precursor cell subpopulations that contribute to murine retinogenesis.Frontiers in cell and developmental biology · 2026Article
- Dicer is essential for proper maturation, composition, and function in the postnatal retina.iScience · 2025Article
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
- A large-scale CRISPR screen reveals context-specific genetic regulation of retinal ganglion cell regeneration.Development (Cambridge, England) · 2024Article
- Sstr2 Defines the Cone Differentiation-Competent Late-Stage Retinal Progenitor Cells in the Developing Mouse Retina.Stem cells translational medicine · 2024Article
- Cell cycle-dependent activation of proneural transcription factor expression and reactive gliosis in rat Müller glia.Scientific reports · 2023Article
- Intrinsic and Induced Neuronal Regeneration in the Mammalian Retina.Antioxidants & redox signaling · 2023Review
- Retinal Ganglion Cell Fate Induction by Ngn-Family Transcription Factors.Investigative ophthalmology & visual science · 2023Article
- The bHLH transcription factor ASCL1 promotes differentiation of endocrine cells in the stomach and is regulated by Notch signaling.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Molecular mechanisms controlling vertebrate retinal patterning, neurogenesis, and cell fate specification.Trends in genetics : TIG · 2023Review
- Overexpressing NeuroD1 reprograms Müller cells into various types of retinal neurons.Neural regeneration research · 2023Article
- Chromatin Remodeling Enzyme Snf2h Is Essential for Retinal Cell Proliferation and Photoreceptor Maintenance.Cells · 2023Article
- Key transcription factors influence the epigenetic landscape to regulate retinal cell differentiation.Nucleic acids research · 2023Article
- Neurog2 regulates Isl1 to modulate horizontal cell number.Development (Cambridge, England) · 2023Article
- Single-Cell Transcriptomic Profiling of Human Retinal Organoids Revealed a Role of IGF1-PHLDA1 Axis in Photoreceptor Precursor Specification.Investigative ophthalmology & visual science · 2022Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms of cell fate diversification in the retina are not fully understood. The seven principal cell types of the neural retina derive from a population of multipotent progenitors during development. These progenitors give rise to multiple cell types concurrently, suggesting that progenitors are a heterogeneous population. It is thought that differences in progenitor gene expression are responsible for differences in progenitor competence (i.e. potential) and, subsequently, fate diversification. To elucidate further the mechanisms of fate diversification, we assayed the expression of three transcription factors made by retinal progenitors: Ascl1 (Mash1), Ngn2 (Neurog2) and Olig2. We observed that progenitors were heterogeneous, expressing every possible combination of these transcription factors. To determine whether this progenitor heterogeneity correlated with different cell fate outcomes, we conducted Ascl1- and Ngn2-inducible expression fate mapping using the CreER™/LoxP system. We found that these two factors gave rise to markedly different distributions of cells. The Ngn2 lineage comprised all cell types, but retinal ganglion cells (RGCs) were exceedingly rare in the Ascl1 lineage. We next determined whether Ascl1 prevented RGC development. Ascl1-null mice had normal numbers of RGCs and, interestingly, we observed that a subset of Ascl1+ cells could give rise to cells expressing Math5 (Atoh7), a transcription factor required for RGC competence. Our results link progenitor heterogeneity to different fate outcomes. We show that Ascl1 expression defines a competence-restricted progenitor lineage in the retina, providing a new mechanism to explain fate diversification.
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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.