ArticleThe EMBO journal2021
Regulated splicing of large exons is linked to phase-separation of vertebrate transcription factors.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
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- The nuclear localization signal of CPSF6 governs post-nuclear import steps of HIV-1 infection.PLoS pathogens · 2025Article
- Evolutionarily Developed Alternatively Spliced Exons Containing Translation Initiation Sites.Cells · 2024Article
- HIV-1 usurps mixed-charge domain-dependent CPSF6 phase separation for higher-order capsid binding, nuclear entry and viral DNA integration.Nucleic acids research · 2024Article
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- The nuclear localization signal of CPSF6 governs post-nuclear import steps of HIV-1 infection.bioRxiv : the preprint server for biology · 2024Article
- Capsid-host interactions for HIV-1 ingress.Microbiology and molecular biology reviews : MMBR · 2023Review
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- Sequence variations of phase-separating proteins and resources for studying biomolecular condensates.Acta biochimica et biophysica Sinica · 2023Review
- Exon Elongation Added Intrinsically Disordered Regions to the Encoded Proteins and Facilitated the Emergence of the Last Eukaryotic Common Ancestor.Molecular biology and evolution · 2023Article
- Pseudogenes and Liquid Phase Separation in Epigenetic Expression.Frontiers in oncology · 2022Review
- Regulated splicing of large exons is linked to phase-separation of vertebrate transcription factors.The EMBO journal · 2021Article
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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
Although large exons cannot be readily recognized by the spliceosome, many are evolutionarily conserved and constitutively spliced for inclusion in the processed transcript. Furthermore, whether large exons may be enriched in a certain subset of proteins, or mediate specific functions, has remained unclear. Here, we identify a set of nearly 3,000 SRSF3-dependent large constitutive exons (S3-LCEs) in human and mouse cells. These exons are enriched for cytidine-rich sequence motifs, which bind and recruit the splicing factors hnRNP K and SRSF3. We find that hnRNP K suppresses S3-LCE splicing, an effect that is mitigated by SRSF3 to thus achieve constitutive splicing of S3-LCEs. S3-LCEs are enriched in genes for components of transcription machineries, including mediator and BAF complexes, and frequently contain intrinsically disordered regions (IDRs). In a subset of analyzed S3-LCE-containing transcription factors, SRSF3 depletion leads to deletion of the IDRs due to S3-LCE exon skipping, thereby disrupting phase-separated assemblies of these factors. Cytidine enrichment in large exons introduces proline/serine codon bias in intrinsically disordered regions and appears to have been evolutionarily acquired in vertebrates. We propose that layered splicing regulation by hnRNP K and SRSF3 ensures proper phase-separation of these S3-LCE-containing transcription factors in vertebrates.
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