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De novo and inherited dominant variants in U4 and U6 snRNA genes cause retinitis pigmentosa

Title: De novo and inherited dominant variants in U4 and U6 snRNA genes cause retinitis pigmentosa
Authors: Quinodoz, M; Rodenburg, K; Cvackova, Z; Kaminska, K; de Bruijn, SE; Iglesias-Romero, AB; Boonen, EGM; Ullah, M; Zomer, N; Folcher, M; Bijon, J; Holtes, LK; Tsang, SH; Corradi, Z; Freund, KB; Shliaga, S; Panneman, DM; Hitti-Malin, RJ; Ali, M; AlTalbishi, A; Andréasson, S; Ansari, G; Arno, G; Astuti, GDN; Charbel Issa, P
Publisher Information: Nature Research
Publication Year: 2026
Collection: Oxford University Research Archive (ORA)
Description: Small nuclear RNAs (snRNAs) combine with specific proteins to generate small nuclear ribonucleoproteins (snRNPs), the building blocks of the spliceosome. U4 snRNA forms a duplex with U6 and, together with U5, contributes to the tri-snRNP spliceosomal complex. Variants in RNU4-2, which encodes U4, have recently been implicated in neurodevelopmental disorders. Here we show that heterozygous inherited and de novo variants in RNU4-2 and in four RNU6 paralogs (RNU6-1, RNU6-2, RNU6-8 and RNU6-9), which encode U6, recur in individuals with nonsyndromic retinitis pigmentosa (RP), a genetic disorder causing progressive blindness. These variants cluster within the three-way junction of the U4/U6 duplex, a site that interacts with tri-snRNP splicing factors also known to cause RP (PRPF3, PRPF8, PRPF31), and seem to affect snRNP biogenesis. Based on our cohort, deleterious variants in RNU4-2 and RNU6 paralogs may explain up to ~1.4% of otherwise undiagnosed RP cases. This study highlights the contribution of noncoding RNA genes to Mendelian disease and reveals pleiotropy in RNU4-2, where distinct variants underlie neurodevelopmental disorder and retinal degeneration.
Document Type: article in journal/newspaper
Language: English
DOI: 10.1038/s41588-025-02451-4
Availability: https://doi.org/10.1038/s41588-025-02451-4; https://ora.ox.ac.uk/objects/uuid:2428ce6c-9be2-4dc6-99f4-53199eeff183
Rights: info:eu-repo/semantics/openAccess ; CC Attribution-NonCommercial-NoDerivatives (CC BY-NC-ND)
Accession Number: edsbas.20E46BC1
Database: BASE