ArticleJCI insight2026
VIRMA modulates function of photoreceptor cells through m6A modification and alternative splicing.
Article in JCI insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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10 authors.
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Abstract
N6-methyladenosine (m6A) modification is the most prevalent posttranscriptional epigenetic modification in mammalian mRNAs, and it has been implicated in the regulation of nervous system development by modulating mRNA metabolism. VIRMA is the largest core subunit of the m6A methyltransferase complex and is essential for the assembly and stability of the m6A methyltransferase complex. In the retina, m6A methylation modification is widely distributed in various cellular layers and is essential for retinal homeostasis. Here, we demonstrate that VIRMA-mediated m6A modification is essential for retinal homeostasis. Loss of Virma in retinal rod cells resulted in abnormal reduction in m6A methylation levels, along with impaired photoreceptor function and degeneration. Mechanically, Virma depletion in photoreceptors dampened the m6A modification level of visual perception-associated genes, resulting compromised visual function and photoreceptors degeneration. Moreover, Virma interacted with splicing factor to regulate the alternative splicing events of retina function-related genes such as Polg2, which contributes to photoreceptor damage. Reintroduction of normal Virma expression colonially rescued photoreceptor degeneration. Collectively, our data elucidate the important role of Virma-mediated m6A modification in photoreceptor function and suggest that epigenetic modulation could serve as a potential target to treat these blinding diseases.
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