ArticleCell death & disease2021
Impaired stem cell differentiation and somatic cell reprogramming in DIDO3 mutants with altered RNA processing and increased R-loop levels.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- 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
- Large-scale exome sequence analysis identifies sex- and age-specific determinants of obesity.Cell genomics · 2023Article
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- Hepatitis, testicular degeneration, and ataxia in DIDO3-deficient mice with altered mRNA processing.Cell & bioscience · 2022Article
- 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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Embryonic stem cell (ESC) differentiation and somatic cell reprogramming are biological processes governed by antagonistic expression or repression of a largely common set of genes. Accurate regulation of gene expression is thus essential for both processes, and alterations in RNA processing are predicted to negatively affect both. We show that truncation of the DIDO gene alters RNA splicing and transcription termination in ESC and mouse embryo fibroblasts (MEF), which affects genes involved in both differentiation and reprogramming. We combined transcriptomic, protein interaction, and cellular studies to identify the underlying molecular mechanism. We found that DIDO3 interacts with the helicase DHX9, which is involved in R-loop processing and transcription termination, and that DIDO3-exon16 deletion increases nuclear R-loop content and causes DNA replication stress. Overall, these defects result in failure of ESC to differentiate and of MEF to be reprogrammed. MEF immortalization restored impaired reprogramming capacity. We conclude that DIDO3 has essential functions in ESC differentiation and somatic cell reprogramming by supporting accurate RNA metabolism, with its exon16-encoded domain playing the main role.
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Registered trials
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.