ArticleBMC developmental biology2010
The long noncoding RNA RNCR2 directs mouse retinal cell specification.
Article in BMC developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.
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Who cites it
113 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
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- The human lncRNA GOMAFU suppresses neuronal interferon response pathways affected in neuropsychiatric diseases.Brain, behavior, and immunity · 2023Article
- The landscape of the long non-coding RNAs in developing mouse retinas.BMC genomics · 2023Article
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- Diabetic Retinopathy: Are lncRNAs New Molecular Players and Targets?Antioxidants (Basel, Switzerland) · 2022Review
- Long non-coding RNA myocardial infarction associated transcript expression and clinical significance in patients with hypertension during pregnancy.Irish journal of medical science · 2022Article
- Miat and interacting protein Metadherin maintain a stem-like niche to promote medulloblastoma tumorigenesis and treatment resistance.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Long Non-coding RNAs: Pivotal Epigenetic Regulators in Diabetic Retinopathy.Current genomics · 2022Review
- The Long Non-Coding RNACells · 2022Review
- Inhibition of the lncRNAMolecular therapy. Nucleic acids · 2022Article
- Rs1894720 polymorphism is associated with the risk of age-related cataract by regulating the proliferation of epithelial cells in the lens via the signalling pathway of MIAT/miR-26b/BCL2L2.Archives of medical science : AMS · 2022Article
53 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
backgroundRecent work has identified that many long mRNA-like noncoding RNAs (lncRNAs) are expressed in the developing nervous system. Despite their abundance, the function of these ncRNAs has remained largely unexplored. We have investigated the highly abundant lncRNA RNCR2 in regulation of mouse retinal cell differentiation.
resultsWe find that the RNCR2 is selectively expressed in a subset of both mitotic progenitors and postmitotic retinal precursor cells. ShRNA-mediated knockdown of RNCR2 results in an increase of both amacrine cells and Müller glia, indicating a role for this lncRNA in regulating retinal cell fate specification. We further report that RNCR2 RNA, which is normally nuclear-retained, can be exported from the nucleus when fused to an IRES-GFP sequence. Overexpression of RNCR2-IRES-GFP phenocopies the effects of shRNA-mediated knockdown of RNCR2, implying that forced mislocalization of RNCR2 induces a dominant-negative phenotype. Finally, we use the IRES-GFP fusion approach to identify specific domains of RNCR2 that are required for repressing both amacrine and Müller glial differentiation.
conclusionThese data demonstrate that the lncRNA RNCR2 plays a critical role in regulating mammalian retinal cell fate specification. Furthermore, we present a novel approach for generating dominant-negative constructs of lncRNAs, which may be generally useful in the functional analysis of this class of molecules.
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Registered trials
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