ArticleMolecular and cellular biology2004
The scl +18/19 stem cell enhancer is not required for hematopoiesis: identification of a 5' bifunctional hematopoietic-endothelial enhancer bound by Fli-1 and Elf-1.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 87 citations in OpenAlex.
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- Genomic Alterations of Non-Coding Regions Underlie Human Cancer: Lessons from T-ALL.Trends in molecular medicine · 2016Review
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- ConBind: motif-aware cross-species alignment for the identification of functional transcription factor binding sites.Nucleic acids research · 2016Article
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- The Hematopoietic Stem and Progenitor Cell Cistrome: GATA Factor-Dependent cis-Regulatory Mechanisms.Current topics in developmental biology · 2016Review
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- The selection and function of cell type-specific enhancers.Nature reviews. Molecular cell biology · 2015Review
- Analysis of hundreds of cis-regulatory landscapes at high resolution in a single, high-throughput experiment.Nature genetics · 2014Article
- Aberrant TAL1 activation is mediated by an interchromosomal interaction in human T-cell acute lymphoblastic leukemia.Leukemia · 2014Article
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- Hard-wired heterogeneity in blood stem cells revealed using a dynamic regulatory network model.Bioinformatics (Oxford, England) · 2013Article
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Authors and funding
16 authors at 4 institutions in 7 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Analysis of cis-regulatory elements is central to understanding the genomic program for development. The scl/tal-1 transcription factor is essential for lineage commitment to blood cell formation and previous studies identified an scl enhancer (the +18/19 element) which was sufficient to target the vast majority of hematopoietic stem cells, together with hematopoietic progenitors and endothelium. Moreover, expression of scl under control of the +18/19 enhancer rescued blood progenitor formation in scl(-/-) embryos. However, here we demonstrate by using a knockout approach that, within the endogenous scl locus, the +18/19 enhancer is not necessary for the initiation of scl transcription or for the formation of hematopoietic cells. These results led to the identification of a bifunctional 5' enhancer (-3.8 element), which targets expression to hematopoietic progenitors and endothelium, contains conserved critical Ets sites, and is bound by Ets family transcription factors, including Fli-1 and Elf-1. These data demonstrate that two geographically distinct but functionally related enhancers regulate scl transcription in hematopoietic progenitors and endothelial cells and suggest that enhancers with dual hematopoietic-endothelial activity may represent a general strategy for regulating blood and endothelial development.
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