ArticleCell death and differentiation2023
General transcription factor TAF4 antagonizes epigenetic silencing by Polycomb to maintain intestine stem cell functions.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- The TAF3/SREBP2/cholesterol axis drives tumor progression in hepatocellular carcinoma.Clinical and experimental medicine · 2026Article
- Systematic analysis of functional genetic and epigenetic variants in colorectal cancer.Science advances · 2026Article
- Molecular and Chromatin Accessibility Programs Underlying Epithelial Injury and Impaired Regeneration in Neonatal Necrotizing Enterocolitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Regulation of NSL by TAF4A is critical for genome stability and quiescence of muscle stem cells.Nature communications · 2025Article
- Nucleolar origins: challenging perspectives on evolution and function.Open biology · 2025Review
- Genetic and microenvironmental evolution of colorectal liver metastases under chemotherapy.Cell reports. Medicine · 2024Article
- Metabolic regulation of intestinal homeostasis: molecular and cellular mechanisms and diseases.MedComm · 2024Review
- Tata-box-binding protein-associated factor 15 as a new potential marker in gastrointestinal tumors.World journal of gastroenterology · 2024Article
- Genomic landscape of diploid and aneuploid microsatellite stable early onset colorectal cancer.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Taf4 (TATA-box binding protein-associated factor 4) is a subunit of the general transcription factor TFIID, a component of the RNA polymerase II pre-initiation complex that interacts with tissue-specific transcription factors to regulate gene expression. Properly regulated gene expression is particularly important in the intestinal epithelium that is constantly renewed from stem cells. Tissue-specific inactivation of Taf4 in murine intestinal epithelium during embryogenesis compromised gut morphogenesis and the emergence of adult-type stem cells. In adults, Taf4 loss impacted the stem cell compartment and associated Paneth cells in the stem cell niche, epithelial turnover and differentiation of mature cells, thus exacerbating the response to inflammatory challenge. Taf4 inactivation ex vivo in enteroids prevented budding formation and maintenance and caused broad chromatin remodeling and a strong reduction in the numbers of stem and progenitor cells with a concomitant increase in an undifferentiated cell population that displayed high activity of the Ezh2 and Suz12 components of Polycomb Repressive Complex 2 (PRC2). Treatment of Taf4-mutant enteroids with a specific Ezh2 inhibitor restored buddings, cell proliferation and the stem/progenitor compartment. Taf4 loss also led to increased PRC2 activity in cells of adult crypts associated with modification of the immune/inflammatory microenvironment that potentiated Apc-driven tumorigenesis. Our results reveal a novel function of Taf4 in antagonizing PRC2-mediated repression of the stem cell gene expression program to assure normal development, homeostasis, and immune-microenvironment of the intestinal epithelium.
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