ArticleCell reports2023
ETV2 primes hematoendothelial gene enhancers prior to hematoendothelial fate commitment.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- TAL1 is indispensable in ETV2-primed human endothelial cell fate determination.Science advances · 2026Article
- Integrated multi-omic atlas reveals the hierarchy of spatiotemporal regulatory networks of mouse gastrulation.Nature communications · 2026Article
- Targeted CRISPR-Cas9 screening identifies core transcription factors controlling murine haemato-endothelial fate commitment.Nature communications · 2025Article
- YAP-Induced Glycolysis Drives Fibroinflammation and Disrupts Fibroblast Fidelity.Circulation research · 2025Article
- The pioneer factor, ETV2, regulates networks to specify the embryonic endothelial lineage.Cardiovascular research · 2025Article
- ETV2 induces endothelial, but not hematopoietic, lineage specification in birds.Life science alliance · 2024Article
- Chromatin priming elements direct tissue-specific gene activity before hematopoietic specification.Life science alliance · 2024Article
- Detecting critical transition signals from single-cell transcriptomes to infer lineage-determining transcription factors.Nucleic acids research · 2022Article
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Mechanisms underlying distinct specification, commitment, and differentiation phases of cell fate determination remain undefined due to difficulties capturing these processes. Here, we interrogate the activity of ETV2, a transcription factor necessary and sufficient for hematoendothelial differentiation, within isolated fate intermediates. We observe transcriptional upregulation of Etv2 and opening of ETV2-binding sites, indicating new ETV2 binding, in a common cardiac-hematoendothelial progenitor population. Accessible ETV2-binding sites are active at the Etv2 locus but not at other hematoendothelial regulator genes. Hematoendothelial commitment coincides with the activation of a small repertoire of previously accessible ETV2-binding sites at hematoendothelial regulators. Hematoendothelial differentiation accompanies activation of a large repertoire of new ETV2-binding sites and upregulation of hematopoietic and endothelial gene regulatory networks. This work distinguishes specification, commitment, and sublineage differentiation phases of ETV2-dependent transcription and suggests that the shift from ETV2 binding to ETV2-bound enhancer activation, not ETV2 binding to target enhancers, drives hematoendothelial fate commitment.
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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.