ArticleNucleic acids research2019
Dido3-dependent SFPQ recruitment maintains efficiency in mammalian alternative splicing.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Multifaceted regulatory role of proline‑ and glutamine-rich splicing factor in tumors (Review).Molecular medicine reports · 2026Review
- Native long-read RNA sequencing of human monocytes reveals activation-induced alternative splicing toward functional isoforms.Nature communications · 2026Article
- Domain acquisition enabled functional expansion of the TFIIS transcription factor family.Cell & bioscience · 2025Review
- The chromatin reader Dido3 is a regulator of the gene network that controls B cell differentiation.Cell & bioscience · 2025Article
- DIDO is necessary for the adipogenesis that promotes diet-induced obesity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- The SPOC proteins DIDO3 and PHF3 co-regulate gene expression and neuronal differentiation.Nature communications · 2023Article
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- The SPOC domain is a phosphoserine binding module that bridges transcription machinery with co- and post-transcriptional regulators.Nature communications · 2023Article
- The Dengue Virus Nonstructural Protein 1 (NS1) Interacts with the Putative Epigenetic Regulator DIDO1 to Promote Flavivirus Replication in Mosquito Cells.Journal of virology · 2022Article
- Hepatitis, testicular degeneration, and ataxia in DIDO3-deficient mice with altered mRNA processing.Cell & bioscience · 2022Article
- Transcriptome analysis of clock disrupted cancer cells reveals differential alternative splicing of cancer hallmarks genes.NPJ systems biology and applications · 2022Article
- Multilayered control of splicing regulatory networks by DAP3 leads to widespread alternative splicing changes in cancer.Nature communications · 2022Article
- SFPQ promotes an oncogenic transcriptomic state in melanoma.Oncogene · 2021Article
- Phosphorylation of H3-Thr3 by Haspin Is Required for Primary Cilia Regulation.International journal of molecular sciences · 2021Article
- Impaired stem cell differentiation and somatic cell reprogramming in DIDO3 mutants with altered RNA processing and increased R-loop levels.Cell death & disease · 2021Article
- A conserved role for the ALS-linked splicing factor SFPQ in repression of pathogenic cryptic last exons.Nature communications · 2021Article
- Systematic profiling of a novel prognostic alternative splicing signature in hepatocellular carcinoma.Oncology reports · 2019Article
- Interplay between splicing and transcriptional pausing exerts genome-wide control over alternative polyadenylation.TranscriptionArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternative splicing is facilitated by accessory proteins that guide spliceosome subunits to the primary transcript. Many of these splicing factors recognize the RNA polymerase II tail, but SFPQ is a notable exception even though essential for mammalian RNA processing. This study reveals a novel role for Dido3, one of three Dido gene products, in alternative splicing. Binding of the Dido3 amino terminus to histones and to the polymerase jaw domain was previously reported, and here we show interaction between its carboxy terminus and SFPQ. We generated a mutant that eliminates Dido3 but preserves other Dido gene products, mimicking reduced Dido3 levels in myeloid neoplasms. Dido mutation suppressed SFPQ binding to RNA and increased skipping for a large group of exons. Exons bearing recognition sequences for alternative splicing factors were nonetheless included more efficiently. Reduced SFPQ recruitment may thus account for increased skipping of SFPQ-dependent exons, but could also generate a splicing factor surplus that becomes available to competing splice sites. Taken together, our data indicate that Dido3 is an adaptor that controls SFPQ utilization in RNA splicing. Distributing splicing factor recruitment over parallel pathways provides mammals with a simple mechanism to regulate exon usage while maintaining RNA splicing efficiency.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.