ArticleInvestigative ophthalmology & visual science2022
Depletion of miR-96 Delays, But Does Not Arrest, Photoreceptor Development in Mice.
Article in Investigative ophthalmology & visual science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- The interplay between form deprivation and dopamine signaling in regulating the expression of circadian rhythm-related genes in the retina of mice.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025Article
- Insight into the role of non-coding RNA in the diagnosis and treatment of retinitis pigmentosa.Non-coding RNA research · 2024Review
- The miR-669a-5p/G3BP/HDAC6/AKAP12 Axis Regulates Primary Cilia Length.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A cell type-specific approach to elucidate the role of miR-96 in inner ear hair cells.Frontiers in audiology and otology · 2024Article
- Dysregulated Arginine Metabolism Is Linked to Retinal Degeneration in Cep250 Knockout Mice.Investigative ophthalmology & visual science · 2023Article
- MicroRNAs in the Mouse Developing Retina.International journal of molecular sciences · 2023Review
- Deletion of histone demethylaseFrontiers in cellular neuroscience · 2023Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Abundant retinal microRNA-183 cluster (miR-183C) has been reported to be a key player in photoreceptor development and functionality in mice. However, whether there is a protagonist in this cluster remains unclear. Here, we used a mutant mouse model to study the role of miR-96, a member of miR-183C, in photoreceptor development and functionality. Methods: The mature miR-96 sequence was removed using the CRISPR/Cas9 genome-editing system. Electroretinogram (ERG) and optical coherence tomography (OCT) investigated the changes in structure and function in mouse retinas. Immunostaining determined the localization and morphology of the retinal cells. RNA sequencing was conducted to observe retinal transcription alterations. Results: The miR-96 mutant mice exhibited cone developmental delay, as occurs in miR-183/96 double knockout mice. Immunostaining of cone-specific marker genes revealed cone nucleus mislocalization and exiguous Opn1mw/Opn1sw in the mutant (MT) mouse outer segments at postnatal day 10. Interestingly, this phenomenon could be relieved in the adult stages. Transcriptome analysis revealed activation of microtubule-, actin filament-, and cilia-related pathways, further supporting the findings. Based on ERG and OCT results at different ages, the MT mice displayed developmental delay not only in cones but also in rods. In addition, a group of miR-96 potential direct and indirect target genes was summarized for interpretation and further studies of miR-96-related retinal developmental defects. Conclusions: Depletion of miR-96 delayed but did not arrest photoreceptor development in mice. This miRNA is indispensable for mouse photoreceptor maturation, especially for cones.
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