ArticleNature communications2025
Identification of human pathways acting on nuclear non-coding RNAs using the Mirror forward genetic approach.
Article in Nature communications, 2025. 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.
- Cell cycle-dependent translation-mediated turnover of the long noncoding RNA Malat1.The Journal of cell biology · 2026Article
- Loss of U11/U12 spliceosome geneLife science alliance · 2026Article
- Harnessing natural RNA triplex elements found in lncRNAs MALAT1 and NEAT1 for engineering of novel riboswitch platforms.Nucleic acids research · 2026Article
- TRNAU1AP and PRPF39 establish integrated control over processing of most abundant human non-coding RNAs.Nature communications · 2026Article
- EXOSC3 G191 Variants Trigger System-Wide Recalibration of RNA Processing Machinery.bioRxiv : the preprint server for biology · 2026Article
- Identification of RMP24 and RMP64, human ribonuclease MRP-specific protein components.Cell reports · 2025Article
- Connecting genotype and phenotype in minor spliceosome diseases.RNA (New York, N.Y.) · 2025Review
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Abstract
Despite critical roles in diseases, human pathways acting on strictly nuclear non-coding RNAs have been refractory to forward genetics. To enable their forward genetic discovery, we developed a single-cell approach that "Mirrors" activities of nuclear pathways with cytoplasmic fluorescence. Application of Mirror to two nuclear pathways targeting MALAT1's 3' end, the pathway of its maturation and the other, the degradation pathway blocked by the triple-helical Element for Nuclear Expression (ENE), identified nearly all components of three complexes: Ribonuclease P and the RNA Exosome, including nuclear DIS3, EXOSC10, and C1D, as well as the Nuclear Exosome Targeting (NEXT) complex. Additionally, Mirror identified DEAD-box helicase DDX59 associated with the genetic disorder Oral-Facial-Digital syndrome (OFD), yet lacking known substrates or roles in nuclear RNA degradation. Knockout of DDX59 exhibits stabilization of the full-length MALAT1 with a stability-compromised ENE and increases levels of 3'-extended forms of small nuclear RNAs. It also exhibits extensive retention of minor introns, including in OFD-associated genes, suggesting a mechanism for DDX59 association with OFD. Mirror efficiently identifies pathways acting on strictly nuclear non-coding RNAs, including essential and indirectly-acting components, and as a result can uncover unexpected links to human disease.
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