ArticleMolecular and cellular neurosciences2013
Heterochronic misexpression of Ascl1 in the Atoh7 retinal cell lineage blocks cell cycle exit.
Article in Molecular and cellular neurosciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Ptbp1 is not required for retinal neurogenesis and cell fate specification.bioRxiv : the preprint server for biology · 2025Article
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
- Article
- Molecular mechanisms controlling vertebrate retinal patterning, neurogenesis, and cell fate specification.Trends in genetics : TIG · 2023Review
- Efficient stimulation of retinal regeneration from Müller glia in adult mice using combinations of proneural bHLH transcription factors.Cell reports · 2021Article
- Genetic control of retinal ganglion cell genesis.Cellular and molecular life sciences : CMLS · 2021Review
- Atoh7-independent specification of retinal ganglion cell identity.Science advances · 2021Article
- Single Cell Transcriptomic Analyses Reveal the Impact of bHLH Factors on Human Retinal Organoid Development.Frontiers in cell and developmental biology · 2021Article
- DACH1 mutation frequency in endometrial cancer is associated with high tumor mutation burden.PloS one · 2020Article
- Integral bHLH factor regulation of cell cycle exit and RGC differentiation.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Article
- All in the family: proneural bHLH genes and neuronal diversity.Development (Cambridge, England) · 2018Review
- Network-based bioinformatics analysis of spatio-temporal RNA-Seq data reveals transcriptional programs underpinning normal and aberrant retinal development.BMC genomics · 2016Article
- Transcriptome of Atoh7 retinal progenitor cells identifies new Atoh7-dependent regulatory genes for retinal ganglion cell formation.Developmental neurobiology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Retinal neurons and glia arise from a common progenitor pool in a temporal order, with retinal ganglion cells (RGCs) appearing first, and Müller glia last. The transcription factors Atoh7/Math5 and Ascl1/Mash1 represent divergent bHLH clades, and exhibit distinct spatial and temporal retinal expression patterns, with little overlap during early development. Here, we tested the ability of Ascl1 to change the fate of cells in the Atoh7 lineage when misexpressed from the Atoh7 locus, using an Ascl1-IRES-DsRed2 knock-in allele. In Atoh7(Ascl1KI/+) and Atoh7(Ascl1KI/Ascl1KI) embryos, ectopic Ascl1 delayed cell cycle exit and differentiation, even in cells coexpressing Atoh7. The heterozygous retinas recovered, and eventually produced a normal complement of RGCs, while homozygous substitution of Ascl1 for Atoh7 did not promote postnatal retinal fates precociously, nor rescue Atoh7 mutant phenotypes. However, our analyses revealed two unexpected findings. First, ectopic Ascl1 disrupted cell cycle progression within the marked Atoh7 lineage, but also nonautonomously in other retinal cells. Second, the size of the Atoh7 retinal lineage was unaffected, supporting the idea of a compensatory shift of the non-proliferative cohort to maintain lineage size. Overall, we conclude that Ascl1 acts dominantly to block cell cycle exit, but is incapable of redirecting the fates of early RPCs.
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