ArticleDevelopment (Cambridge, England)2013
Notch1 is required in newly postmitotic cells to inhibit the rod photoreceptor fate.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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Who cites it
41 citing papers in PubMed, 76 citations in OpenAlex.
- Placental Extracellular Vesicles Exhibit Reduced Neurogenic Potential Linked to Changes in Their miRNA Landscape Upon HCMV Infection.Journal of extracellular biology · 2026Article
- Development of Retinal Astroglia.Annual review of vision science · 2025Review
- Expression status transition ofF1000Research · 2025Article
- Robust reprogramming of glia into neurons by inhibition of Notch signaling and nuclear factor I (NFI) factors in adult mammalian retina.Science advances · 2024Article
- Article
- Retinal Ganglion Cell Fate Induction by Ngn-Family Transcription Factors.Investigative ophthalmology & visual science · 2023Article
- 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
- Key transcription factors influence the epigenetic landscape to regulate retinal cell differentiation.Nucleic acids research · 2023Article
- Boolean implication analysis of single-cell data predicts retinal cell type markers.BMC bioinformatics · 2022Article
- Timed Notch Inhibition Drives Photoreceptor Fate Specification in Human Retinal Organoids.Investigative ophthalmology & visual science · 2022Article
- Ciliary photoreceptors in sea urchin larvae indicate pan-deuterostome cell type conservation.BMC biology · 2021Article
- Notch signaling represses cone photoreceptor formation through the regulation of retinal progenitor cell states.Scientific reports · 2021Article
- ID1 and ID3 are Negative Regulators of TGFβ2-Induced Ocular Hypertension and Compromised Aqueous Humor Outflow Facility in Mice.Investigative ophthalmology & visual science · 2021Article
- Genetic control of retinal ganglion cell genesis.Cellular and molecular life sciences : CMLS · 2021Review
- Müller Glia in Retinal Development: From Specification to Circuit Integration.Frontiers in neural circuits · 2021Review
- Zeb2 regulates the balance between retinal interneurons and Müller glia by inhibition of BMP-Smad signaling.Developmental biology · 2020Article
- Reprogramming Müller Glia to Regenerate Retinal Neurons.Annual review of vision science · 2020Review
- Extension of the Notch intracellular domain ankyrin repeat stack by NRARP promotes feedback inhibition of Notch signaling.Science signaling · 2019Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Several models of cell fate determination can be invoked to explain how single retinal progenitor cells (RPCs) produce different cell types in a terminal division. To gain insight into this process, the effects of the removal of a cell fate regulator, Notch1, were studied in newly postmitotic cells using a conditional allele of Notch1 (N1-CKO) in mice. Almost all newly postmitotic N1-CKO cells became rod photoreceptors, whereas wild-type (WT) cells achieved a variety of fates. Single cell profiling of wild-type and N1-CKO retinal cells transitioning from progenitor to differentiated states revealed differential expression of inhibitor of DNA binding factors Id1 and Id3, as well as Notch-regulated ankyrin repeat protein (Nrarp). Misexpression of Id1 and Id3 was found to be sufficient to drive production of Müller glial cells and/or RPCs. Moreover, Id1 and Id3 were shown to partially rescue the production of bipolar and Müller glial cells in the absence of Notch1 in mitotic and newly postmitotic cells. Misexpression of Nrarp, a downstream target gene and inhibitor of the Notch signaling pathway, resulted in the overproduction of rod photoreceptors at the expense of Müller glial cells. These data demonstrate that cell fate decisions can be made in newly postmitotic retinal cells, and reveal some of the regulators downstream of Notch1 that influence the choice of rod and non-rod fates. Taken together, our results begin to address how different signals downstream from a common pathway lead to different fate outcomes.
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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.