<i>Ngn3</i> Regulates Differentiation Competence of Retinal Progenitor Cells Through Transcriptional and Epigenetic Modification.
Overview
Abstract
The retina is a complex sensory neural tissue composed of six major types of neurons and one type of glial cell. The cell fate specification of retinal cells is tightly governed by intrinsic factors and extrinsic microenvironmental cues. Among the key regulators directing retinal cell fate differentiation is a group of bHLH family transcription factors (TFs). Our previous work demonstrated that the bHLH TF Ngn3 exhibits robust potential to induce retinogenesis in both distantly related fibroblasts in vitro and late retinal progenitor cells (RPCs) in vivo. However, the underlying molecular mechanisms remain largely elusive. In this study, we combined immunohistological examination and RNA-seq and ATAC-seq analyses to investigate the cellular and molecular mechanisms governing Ngn3-driven retinogenesis in late RPCs. Our results revealed that Ngn3 overexpression promotes premature cell cycle exit in late RPCs and remodels their transcriptomic and epigenomic landscape towards a state favoring rod photoreceptor and RGC differentiation. Furthermore, cross-comparison with Ngn3-overexpressing fibroblasts in vitro revealed cell-type-specific mechanisms underlying Ngn3-mediated neuronal fate reprogramming. These findings advance our understanding of Ngn family-mediated retinal cell fate regulation and provide a mechanistic framework for optimizing Ngn3-based retinal regeneration strategies for the treatment of retinal degeneration diseases.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE326387, at NCBI GEO; found in “Data Availability Statement”
Other data links
- ncbi.nlm.nih.gov/
geo , NCBI; found in “Data Availability Statement”
Data Availability Statement
The original data presented in the study are openly available in GEO under at https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 30 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 4 authors, 6 keywords, 9 MeSH terms, 2 funders, 28 references.
Cite
This paper
Chen, C., Liang, H., He, Q., & Chen, S. (2026). &
BibTeX
@article{chen2026lt,
author = {Chen, Canbin and Liang, Huilin and He, Qinghai and Chen, Shuyi},
title = {{\&
journal = {International journal of molecular sciences},
year = {2026},
month = apr,
volume = {27},
number = {9},
pages = {3845},
publisher = {Multidisciplinary Digital Publishing Institute (MDPI)},
issn = {1422-0067},
doi = {10.3390/
url = {https://
pmid = {42123429},
pmcid = {PMC13164411}
}
RIS
TY - JOUR
AU - Chen, Canbin
AU - Liang, Huilin
AU - He, Qinghai
AU - Chen, Shuyi
TI - &
T2 - International journal of molecular sciences
J2 - Int J Mol Sci
PY - 2026
DA - 2026/
VL - 27
IS - 9
SP - 3845
SN - 1422-0067
PB - Multidisciplinary Digital Publishing Institute (MDPI)
DO - 10.3390/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.3390/
"type": "article-journal",
"title": "&
"container-title": "International journal of molecular sciences",
"author": [
{
"family": "Chen",
"given": "Canbin"
},
{
"family": "Liang",
"given": "Huilin"
},
{
"family": "He",
"given": "Qinghai"
},
{
"family": "Chen",
"given": "Shuyi"
}
],
"container-title-short":
"volume": "27",
"issue": "9",
"page": "3845",
"DOI": "10.3390/
"PMID": "42123429",
"PMCID": "PMC13164411",
"ISSN": "1422-0067",
"publisher": "Multidisciplinary Digital Publishing Institute (MDPI)",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
26
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1167/iovs.67.10.41
- Ascl1 Represses Müller Glial and Promotes Rod Photoreceptor Fate Through Repressing Notch Signaling in Late Retinal Progenitor Cells.Journal: Investigative ophthalmology & visual scienceIn common: genetics / omics, mouse, cellular / molecular, 7 references
- [2] doi:10.1016/j.stemcr.2026.103004
- Induction of human pruriceptors from pluripotent stem cells via transcription factors.Journal: Stem cell reportsIn common: cellular / molecular, 3 references
- [3] doi:10.1167/iovs.67.6.9 [code]
- Stress Responsive bZIP Transcription Factors ATF4 and BACH1 Cooperate With MAF-Family bZIP Protein NRL to Fine-Tune Rod Photoreceptor Gene Expression.Journal: Investigative ophthalmology & visual scienceIn common: genetics / omics, mouse, cellular / molecular, 2 references
- [4] doi:10.1038/s41467-026-71619-1
- Structurally exclusive Teneurin complexes orchestrate divergent programs in early cortical development.Journal: Nature communicationsIn common: mouse, 2 references
- [5] doi:10.1002/imt2.70163 [code]
- Spatial multi-omics unveils sphingolipid metabolic reprogramming within the retinal pathological niche.Journal: iMetaIn common: genetics / omics, mouse, cellular / molecular, 1 reference
- [6] doi:10.1371/journal.pbio.3003931 [code]
- A single-cell transcriptomic atlas reveals the emergence of medusa-specific cell states in the scyphozoan Aurelia coerulea.Journal: PLoS biologyIn common: genetics / omics, cellular / molecular, 1 reference
- [7] doi:10.1126/sciadv.aeg3223 [code]
- The extreme diversity of retinal amacrine cells has deep evolutionary roots.Journal: Science advancesIn common: genetics / omics, cellular / molecular, 1 reference
- [8] doi:10.1038/s41597-026-07173-8 [code]
- The Cell Ontology in the age of single-cell omics.Journal: Scientific dataIn common: genetics / omics, cellular / molecular, 1 reference
- [9] doi:10.1126/sciadv.aee4940 [code]
- Neuron-derived SPP1 instructs microglia to limit degeneration.Journal: Science advancesIn common: mouse, cellular / molecular, 1 reference
- [10] doi:10.1242/dev.204980 [code]
- PTEN regulates starburst amacrine cell dendrite morphology during development.Journal: Development (Cambridge, England)In common: mouse, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.