ArticleNature communications2024
The debranching enzyme Dbr1 regulates lariat turnover and intron splicing.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Emerging strategies and innovations in circular RNA synthesis.Molecular therapy. Nucleic acids · 2026Review
- Mechanism of spliceosome termination.Nature · 2026Article
- A genome-scale CRISPRi perturbation atlas of human induced pluripotent stem cells.Nature biotechnology · 2026Article
- The human DBR1 interactome reveals coupling between intron lariat turnover, pre-mRNA splicing, and RNA quality control pathways.Cell stress & chaperones · 2026Article
- Defects in intron recycling suppress the antiviral response via a mechanism of intronic endogenous dsRNA.The Journal of experimental medicine · 2026Article
- Therapeutic microRNAs: Mechanisms, Delivery, and Clinical Translation in Oncology.International journal of molecular sciences · 2026Review
- SPLiCR-seq: A CRISPR-Based Screening Platform for RNA splicing Identifies Novel Regulators of IRE1α-XBP1 Signaling Under ER Stress.Nature communications · 2025Article
- Cryptic intronic transcriptional initiation generates efficient endogenous mRNA templates for C9orf72-associated RAN translation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The pre-mRNA splicing modulator pladienolide B inhibitsmSphere · 2025Article
- DBR1 orchestrates the fate of lariat RNA: debranching-dependent turnover and function.Nucleic acids research · 2025Review
- Regulatory mechanism of circular RNAs in brain and neurodegenerative diseases.Frontiers in molecular neuroscience · 2025Review
- Intron lariat spliceosomes convert lariats to true circles: implications for intron transposition.Genes & development · 2024Article
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16 authors.
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Abstract
The majority of genic transcription is intronic. Introns are removed by splicing as branched lariat RNAs which require rapid recycling. The branch site is recognized during splicing catalysis and later debranched by Dbr1 in the rate-limiting step of lariat turnover. Through generation of a viable DBR1 knockout cell line, we find the predominantly nuclear Dbr1 enzyme to encode the sole debranching activity in human cells. Dbr1 preferentially debranches substrates that contain canonical U2 binding motifs, suggesting that branchsites discovered through sequencing do not necessarily represent those favored by the spliceosome. We find that Dbr1 also exhibits specificity for particular 5' splice site sequences. We identify Dbr1 interactors through co-immunoprecipitation mass spectrometry. We present a mechanistic model for Dbr1 recruitment to the branchpoint through the intron-binding protein AQR. In addition to a 20-fold increase in lariats, Dbr1 depletion increases exon skipping. Using ADAR fusions to timestamp lariats, we demonstrate a defect in spliceosome recycling. In the absence of Dbr1, spliceosomal components remain associated with the lariat for a longer period of time. As splicing is co-transcriptional, slower recycling increases the likelihood that downstream exons will be available for exon skipping.
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