ArticleNeural development2014
Establishment of the neurogenic boundary of the mouse retina requires cooperation of SOX2 and WNT signaling.
Article in Neural development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Ezh2 Control of Bivalent Genes Fine-Tunes Developmental Competence During Retinogenesis.Investigative ophthalmology & visual science · 2026Article
- SOX2-VSX2 Co-Occupancy Shapes Retinal Neurogenesis Through Dynamic Chromatin Regulation.bioRxiv : the preprint server for biology · 2025Article
- SOX2-driven enhancer landscape defines the transcriptional architecture of retinogenesis.Development (Cambridge, England) · 2024Article
- Article
- Molecular basis for SOX2-dependent regulation of super-enhancer activity.Nucleic acids research · 2023Article
- Molecular mechanisms controlling vertebrate retinal patterning, neurogenesis, and cell fate specification.Trends in genetics : TIG · 2023Review
- Article
- Phase transition specified by a binary code patterns the vertebrate eye cup.Science advances · 2021Article
- Article
- Embryology, Malformations, and Rare Diseases of the Cochlea.Laryngo- rhino- otologie · 2021Article
- Meis homeobox genes control progenitor competence in the retina.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The transcription factorDisease models & mechanisms · 2020Article
- Functional characterization of SOX2 as an anticancer target.Signal transduction and targeted therapy · 2020Review
- Pluripotent Stem Cells for the Treatment of Retinal Degeneration: Current Strategies and Future Directions.Frontiers in cell and developmental biology · 2020Review
- Low availability of cholineFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- The peripheral eye: A neurogenic area with potential to treat retinal pathologies?Progress in retinal and eye research · 2019Review
- Up-regulation of microRNA-200c-3p inhibits invasion and migration of renal cell carcinoma cells via the SOX2-dependent Wnt/β-catenin signaling pathway.Cancer cell international · 2019Article
- In Vivo Evaluation of PAX6 Overexpression and NMDA Cytotoxicity to Stimulate Proliferation in the Mouse Retina.Scientific reports · 2018Article
- SOX2 haploinsufficiency promotes impaired vision at advanced age.Oncotarget · 2018Article
- Six3 and Six6 Are Jointly Required for the Maintenance of Multipotent Retinal Progenitors through Both Positive and Negative Regulation.Cell reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEye development in vertebrates relies on the critical regulation of SOX2 expression. Humans with mutations in SOX2 often suffer from eye defects including anophthalmia (no eye) and microphthalmia (small eye). In mice, deletion of Sox2 in optic cup progenitor cells results in loss of neural competence and cell fate conversion of the neural retina to a non-neurogenic fate, specifically the acquisition of fate associated with progenitors of the ciliary epithelium. This fate is also promoted with constitutive expression of stabilized β-Catenin in the optic cup, where the WNT pathway is up-regulated. We addressed whether SOX2 co-ordinates the neurogenic boundary of the retina through modulating the WNT/β-Catenin pathway by using a genetic approach in the mouse.
resultsUpon deletion of Sox2 in the optic cup, response to WNT signaling was expanded, correlating with loss of neural competence, cell fate conversion of the neural retina to ciliary epithelium primordium and, in addition, increased cell cycle time of optic cup progenitors. Removal of Ctnnb1 rescued the cell fate conversion; however, the loss of neural competence and the proliferation defect resulting from lack of SOX2 were not overcome. Lastly, central Sox2-deficient optic cup progenitor cells exhibited WNT-independent up-regulation of D-type Cyclins.
conclusionWe propose two distinct roles for SOX2 in the developing retina. Our findings suggest that SOX2 antagonizes the WNT pathway to maintain a neurogenic fate and, in contrast, regulates cycling of optic cup progenitors in a WNT-independent manner. Given that WNT signaling acting upstream of SOX2 has been implicated in the tumorigenicity of embryonic stem cell-derived retinal progenitor cells, our results distinguish the endogenous role of WNT signaling in early optic cup patterning and support a WNT-independent role for SOX2 in maintaining retinal progenitor cell proliferation.
Indexed as
Identifiers
What OpenQuestion holds
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.