ArticleScientific reports2016
Histone modifications and p53 binding poise the p21 promoter for activation in human embryonic stem cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- PRAMEY enhances sperm-egg binding and modulates epigenetic dynamics in bovine embryogenesis.Cell and tissue research · 2025Article
- Hypoxia-induced increase in sphingomyelin synthase 2 aggravates ischemic skeletal muscle inflammation.The FEBS journal · 2025Article
- Diphthamide deficiency promotes association of eEF2 with p53 to induce p21 expression and neural crest defects.Nature communications · 2024Article
- Review
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- Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.International journal of molecular sciences · 2021Review
- Tau Stabilizes Chromatin Compaction.Frontiers in cell and developmental biology · 2021Article
- Article
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- A novel member of Prame family, Gm12794c, counteracts retinoic acid differentiation through the methyltransferase activity of PRC2.Cell death and differentiation · 2020Article
- Cellular responses to ionizing radiation change quickly over time during early development in zebrafish.Cell biology international · 2019Article
- Emerging Roles of p53 Family Members in Glucose Metabolism.International journal of molecular sciences · 2018Review
- Ceramide Signaling and p53 Pathways.Advances in cancer research · 2018Review
- Cell cycle and pluripotency: Convergence on octamer‑binding transcription factor 4 (Review).Molecular medicine reports · 2017Review
- Putting p53 in Context.Cell · 2017Review
- Emerging Non-Canonical Functions and Regulation by p53: p53 and Stemness.International journal of molecular sciences · 2016Review
- Iterative Fragmentation Improves the Detection of ChIP-seq Peaks for Inactive Histone Marks.Bioinformatics and biology insights · 2016Article
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Authors and funding
11 authors.
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Abstract
The high proliferation rate of embryonic stem cells (ESCs) is thought to arise partly from very low expression of p21. However, how p21 is suppressed in ESCs has been unclear. We found that p53 binds to the p21 promoter in human ESCs (hESCs) as efficiently as in differentiated human mesenchymal stem cells, however it does not promote p21 transcription in hESCs. We observed an enrichment for both the repressive histone H3K27me3 and activating histone H3K4me3 chromatin marks at the p21 locus in hESCs, suggesting it is a suppressed, bivalent domain which overrides activation by p53. Reducing H3K27me3 methylation in hESCs rescued p21 expression, and ectopic expression of p21 in hESCs triggered their differentiation. Further, we uncovered a subset of bivalent promoters bound by p53 in hESCs that are similarly induced upon differentiation in a p53-dependent manner, whereas p53 promotes the transcription of other target genes which do not show an enrichment of H3K27me3 in ESCs. Our studies reveal a unique epigenetic strategy used by ESCs to poise undesired p53 target genes, thus balancing the maintenance of pluripotency in the undifferentiated state with a robust response to differentiation signals, while utilizing p53 activity to maintain genomic stability and homeostasis in ESCs.
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