ArticleNature cell biology2020
Haematopoietic stem cell-dependent Notch transcription is mediated by p53 through the Histone chaperone Supt16h.
Article in Nature cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- SUPT16H-associated neurodevelopmental disorder and neurocristopathy: genetic and phenotypic spectrum.Human molecular genetics · 2026Article
- Insights into FACT in Cancers with Targeted Therapeutic Implications.Molecular and cellular biology · 2026Review
- Molecular mechanisms of thymopoietin in papillary thyroid cancer: Multiplatform gene expression data, gene knockout screening, and in-house immunohistochemistry.World journal of clinical oncology · 2025Article
- SMC2 and Condensin II Subunits Are Essential for the Development of Hematopoietic Stem and Progenitor Cells in Zebrafish.Journal of cellular physiology · 2025Article
- Article
- Exploring hematopoiesis in zebrafish using forward genetic screening.Experimental & molecular medicine · 2024Review
- FACT regulates pluripotency through proximal and distal regulation of gene expression in murine embryonic stem cells.BMC biology · 2023Article
- The fly homolog of SUPT16H, a gene associated with neurodevelopmental disorders, is required in a cell-autonomous fashion for cell survival.Human molecular genetics · 2023Article
- The Contribution of the Zebrafish Model to the Understanding of Polycomb Repression in Vertebrates.International journal of molecular sciences · 2023Review
- Transgenic fluorescent zebrafish lines that have revolutionized biomedical research.Laboratory animal research · 2021Review
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 2 countries.
Funding
Abstract
Haematopoietic stem and progenitor cells (HSPCs) have been the focus of developmental and regenerative studies, yet our understanding of the signalling events regulating their specification remains incomplete. We demonstrate that supt16h, a component of the Facilitates chromatin transcription (FACT) complex, is required for HSPC formation. Zebrafish supt16h mutants express reduced levels of Notch-signalling components, genes essential for HSPC development, due to abrogated transcription. Whereas global chromatin accessibility in supt16h mutants is not substantially altered, we observe a specific increase in p53 accessibility, causing an accumulation of p53. We further demonstrate that p53 influences expression of the Polycomb-group protein PHC1, which functions as a transcriptional repressor of Notch genes. Suppression of phc1 or its upstream regulator, p53, rescues the loss of both Notch and HSPC phenotypes in supt16h mutants. Our results highlight a relationship between supt16h, p53 and phc1 to specify HSPCs via modulation of Notch signalling.
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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.