ArticleNature communications2018
SCL/TAL1 cooperates with Polycomb RYBP-PRC1 to suppress alternative lineages in blood-fated cells.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Human Hematopoietic Stem Cells Enhance Maturational Differentiation of hiPSC-Derived Cardiomyocytes on Xeno-Free MatriClone-Plastic via EGFR/MAPK/ERK Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Role of SLC Transporters and Noncoding RNA in Regulating the Genetic Landscape of the Blood Disorders.Experientia supplementum (2012) · 2026Review
- MAP3K3 Contributes to Myocardial Ischemia/Reperfusion Injury by Promoting Myeloid Cell Diapedesis through TAL1/JAM-A Pathway.Theranostics · 2026Article
- Competing dynamic gene regulatory networks involved in fibroblast reprogramming to hematopoietic progenitor cells.Stem cell reports · 2025Article
- Leveraging neighborhood representations of single-cell data to achieve sensitive DE testing with miloDE.Genome biology · 2024Article
- Transcription Factor TAL1 in Erythropoiesis.Advances in experimental medicine and biology · 2024Review
- Research advances of polycomb group proteins in regulating mammalian development.Frontiers in cell and developmental biology · 2024Review
- Engineered hematopoietic and immune cells derived from human pluripotent stem cells.Experimental hematology · 2023Review
- Sensitive cluster-free differential expression testing.bioRxiv : the preprint server for biology · 2023Article
- De Novo Generation of Human Hematopoietic Stem Cells from Pluripotent Stem Cells for Cellular Therapy.Cells · 2023Review
- Identifying a novel role for the master regulator Tal1 in the Endothelial to Hematopoietic Transition.Scientific reports · 2022Article
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- H3K27me3 conditions chemotolerance in triple-negative breast cancer.Nature genetics · 2022Article
- Article
- Scalable in vitro production of defined mouse erythroblasts.PloS one · 2022Article
- The migratory pathways of the cells that form the endocardium, dorsal aortae, and head vasculature in the mouse embryo.BMC developmental biology · 2021Article
- Reduction of RUNX1 transcription factor activity by a CBFA2T3-mimicking peptide: application to B cell precursor acute lymphoblastic leukemia.Journal of hematology & oncology · 2021Article
- The T-box transcription factor Eomesodermin governs haemogenic competence of yolk sac mesodermal progenitors.Nature cell biology · 2021Article
- The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis.Scientific reports · 2020Article
- Single-cell fate decisions of bipotential hematopoietic progenitors.Current opinion in hematology · 2020Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 3 countries.
Funding
Abstract
During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood (Scl/Tal1), cardiac (Mesp1) and paraxial (Tbx6) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl-null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes.
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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.