ArticleDevelopmental biology2012
Math5 defines the ganglion cell competence state in a subpopulation of retinal progenitor cells exiting the cell cycle.
Article in Developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 147 citations in OpenAlex.
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- Human pluripotent stem cell-derived retinal ganglion cells: advances in differentiation and translational applications.Molecular medicine (Cambridge, Mass.) · 2025Review
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- Sstr2 Defines the Cone Differentiation-Competent Late-Stage Retinal Progenitor Cells in the Developing Mouse Retina.Stem cells translational medicine · 2024Article
- Forced MyD88 signaling in microglia impacts the production and survival of regenerated retinal neurons.Frontiers in cell and developmental biology · 2024Article
- Intrinsic and Induced Neuronal Regeneration in the Mammalian Retina.Antioxidants & redox signaling · 2023Review
- Therapeutic strategies for glaucoma and optic neuropathies.Molecular aspects of medicine · 2023Review
- Molecular mechanisms controlling vertebrate retinal patterning, neurogenesis, and cell fate specification.Trends in genetics : TIG · 2023Review
- Notch pathway mutants do not equivalently perturb mouse embryonic retinal development.PLoS genetics · 2023Article
- InducibleCells · 2023Article
- Inducing Neural Regeneration from Glia Using Proneural bHLH Transcription Factors.Advances in experimental medicine and biology · 2023Review
- Directly induced human retinal ganglion cells mimic fetal RGCs and are neuroprotective after transplantation in vivo.Stem cell reports · 2022Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The basic helix-loop-helix (bHLH) transcription factor Math5 (Atoh7) is transiently expressed during early retinal histogenesis and is necessary for retinal ganglion cell (RGC) development. Using nucleoside pulse-chase experiments and clonal analysis, we determined that progenitor cells activate Math5 during or after the terminal division, with progressively later onset as histogenesis proceeds. We have traced the lineage of Math5+ cells using mouse BAC transgenes that express Cre recombinase under strict regulatory control. Quantitative analysis showed that Math5+ progenitors express equivalent levels of Math5 and contribute to every major cell type in the adult retina, but are heavily skewed toward early fates. The Math5>Cre transgene labels 3% of cells in adult retina, including 55% of RGCs. Only 11% of Math5+ progenitors develop into RGCs; the majority become photoreceptors. The fate bias of the Math5 cohort, inferred from the ratio of cone and rod births, changes over time, in parallel with the remaining neurogenic population. Comparable results were obtained using Math5 mutant mice, except that ganglion cells were essentially absent, and late fates were overrepresented within the lineage. We identified Math5-independent RGC precursors in the earliest born (embryonic day 11) retinal cohort, but these precursors require Math5-expressing cells for differentiation. Math5 thus acts permissively to establish RGC competence within a subset of progenitors, but is not sufficient for fate specification. It does not autonomously promote or suppress the determination of non-RGC fates. These data are consistent with progressive and temporal restriction models for retinal neurogenesis, in which environmental factors influence the final histotypic choice.
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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.