ArticleNucleic acids research2020
A splice site-sensing conformational switch in U2AF2 is modulated by U2AF1 and its recurrent myelodysplasia-associated mutation.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- REAL-TIME VISUALIZATION OF SPLICEOSOME ASSEMBLY REVEALS BASIC PRINCIPLES OF 3' SPLICE SITE SELECTION.Research square · 2026Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.Nature genetics · 2026Article
- OTUB2-mediated deubiquitination upregulates U2AF2 to promote colorectal cancer evasion of autophagy-ferroptosis.Cell death & disease · 2026Article
- Phosphorylation-dependent regulation of serine/arginine-rich proteins and U2AF1 interactions in early spliceosome assembly.The Journal of biological chemistry · 2026Article
- Genome-wide modulation of alternative splicing by a predicted alpha helix in U2AF2.Nucleic acids research · 2025Article
- HPGD induces ferroptosis and autophagy to suppress esophageal squamous cell carcinoma through the LXA4-ERK1/2-U2AF2-TFRC axis.Molecular cancer · 2025Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.bioRxiv : the preprint server for biology · 2025Article
- Revealing the role of U2AF1 in splicing regulation and chimeric RNA dynamics.Scientific reports · 2025Article
- C9orf72-linked arginine-rich dipeptide repeats aggravate pathological phase separation of G3BP1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular impact of mutations in RNA splicing factors in cancer.Molecular cell · 2024Review
- Development and validation of AI/ML derived splice-switching oligonucleotides.Molecular systems biology · 2024Article
- Understanding YTHDF2-mediated mRNA degradation by m6A-BERT-Deg.Briefings in bioinformatics · 2024Article
- Exonic splicing code and coordination of divalent metals in proteins.Nucleic acids research · 2024Article
- Article
- Improved analysis of (e)CLIP data with RCRUNCH yields a compendium of RNA-binding protein binding sites and motifs.Genome biology · 2023Article
- Profiling lariat intermediates reveals genetic determinants of early and late co-transcriptional splicing.Molecular cell · 2022Article
- Cytogenetic and Genetic Abnormalities with Diagnostic Value in Myelodysplastic Syndromes (MDS): Focus on the Pre-Messenger RNA Splicing Process.Diagnostics (Basel, Switzerland) · 2022Review
- Pre-mRNA splicing factor U2AF2 recognizes distinct conformations of nucleotide variants at the center of the pre-mRNA splice site signal.Nucleic acids research · 2022Article
- Review
- Precision analysis of mutant U2AF1 activity reveals deployment of stress granules in myeloid malignancies.Molecular cell · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
An essential heterodimer of the U2AF1 and U2AF2 pre-mRNA splicing factors nucleates spliceosome assembly at polypyrimidine (Py) signals preceding the major class of 3' splice sites. U2AF1 frequently acquires an S34F-encoding mutation among patients with myelodysplastic syndromes (MDS). The influence of the U2AF1 subunit and its S34F mutation on the U2AF2 conformations remains unknown. Here, we employ single molecule Förster resonance energy transfer (FRET) to determine the influence of wild-type or S34F-substituted U2AF1 on the conformational dynamics of U2AF2 and its splice site RNA complexes. In the absence of RNA, the U2AF1 subunit stabilizes a high FRET value, which by structure-guided mutagenesis corresponds to a closed conformation of the tandem U2AF2 RNA recognition motifs (RRMs). When the U2AF heterodimer is bound to a strong, uridine-rich splice site, U2AF2 switches to a lower FRET value characteristic of an open, side-by-side arrangement of the RRMs. Remarkably, the U2AF heterodimer binds weak, uridine-poor Py tracts as a mixture of closed and open U2AF2 conformations, which are modulated by the S34F mutation. Shifts between open and closed U2AF2 may underlie U2AF1-dependent splicing of degenerate Py tracts and contribute to a subset of S34F-dysregulated splicing events in MDS patients.
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