ArticleMolecular and cellular biology2001
Reconstitution of human beta-globin locus control region hypersensitive sites in the absence of chromatin assembly.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Enhancer-Mediated Formation of Nuclear Transcription Initiation Domains.International journal of molecular sciences · 2022Review
- Super-enhancer mediated regulation of adult β-globin gene expression: the role of eRNA and Integrator.Nucleic acids research · 2021Article
- Coordination of transcription, processing, and export of highly expressed RNAs by distinct biomolecular condensates.Emerging topics in life sciences · 2020Article
- An intergenic non-coding RNA promoter required for histone modifications in the human β-globin chromatin domain.PloS one · 2019Article
- Transvection-like interchromosomal interaction is not observed at the transcriptional level when tested in the Rosa26 locus in mouse.PloS one · 2019Article
- Phase Separation and Transcription Regulation: Are Super-Enhancers and Locus Control Regions Primary Sites of Transcription Complex Assembly?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Review
- Identification of a Novel Enhancer/Chromatin Opening Element Associated with High-Level γ-Globin Gene Expression.Molecular and cellular biology · 2018Article
- High Fractional Occupancy of a Tandem Maf Recognition Element and Its Role in Long-Range β-Globin Gene Regulation.Molecular and cellular biology · 2016Article
- Genomic and proteomic analysis of transcription factor TFII-I reveals insight into the response to cellular stress.Nucleic acids research · 2014Article
- Dissecting the function of the adult β-globin downstream promoter region using an artificial zinc finger DNA-binding domain.Nucleic acids research · 2014Article
- Chromatin states reveal functional associations for globally defined transcription start sites in four human cell lines.BMC genomics · 2014Article
- The emerging roles of eRNAs in transcriptional regulatory networks.RNA biology · 2014Article
- Promoter cross-talk via a shared enhancer explains paternally biased expression of Nctc1 at the Igf2/H19/Nctc1 imprinted locus.Nucleic acids research · 2013Article
- Recruitment of transcription complexes to enhancers and the role of enhancer transcription.Biology · 2012Article
- Neutralizing the function of a β-globin-associated cis-regulatory DNA element using an artificial zinc finger DNA-binding domain.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Transcription factor binding at enhancers: shaping a genomic regulatory landscape in flux.Frontiers in genetics · 2012Article
- Review
- USF and NF-E2 cooperate to regulate the recruitment and activity of RNA polymerase II in the beta-globin gene locus.The Journal of biological chemistry · 2010Article
- Defective erythropoiesis in transgenic mice expressing dominant-negative upstream stimulatory factor.Molecular and cellular biology · 2009Article
- Locus control region mediated regulation of adult beta-globin gene expression.Journal of cellular biochemistry · 2008Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The human beta-globin genes are regulated by the locus control region (LCR), an element composed of multiple DNase I-hypersensitive sites (HS sites) located 5' to the genes. Various functional studies indicate that the LCR confers high-level, position-independent, and copy number-dependent expression to linked globin genes in transgenic mice. However, the structural basis for LCR function is unknown. Here we show that LCR HS sites can be reconstituted in an erythroid cell-specific manner on chromatin-assembled LCR templates in vitro. Surprisingly, HS2 and HS3 are also formed with erythroid proteins in the absence of chromatin assembly, indicating that sensitivity to nucleases is not simply a consequence of nucleosome reorganization. The generation of LCR HS sites in the absence of chromatin assembly leads to the formation of S1- and KMnO(4)-sensitive regions in HS2 and HS3. These sites are also sensitive to S1 nuclease in erythroid cells in vivo, suggesting a distorted DNA structure in the LCR core enhancer elements. Finally, we show that RNA polymerase II initiates transcription in the HS2 and HS3 core enhancer regions in vitro. Transcription in both HS2 and HS3 proceeds in a unidirectional manner. Taken together, the data suggest that erythroid proteins interact with the core enhancer elements, distort the DNA structure, and recruit polymerase II transcription complexes. These results further our understanding of the structural basis for LCR function and provide an explanation for why the LCR core regions are so extremely sensitive to nucleases in erythroid cells.
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