Dynamic Regulation of Nucleosome Positioning in the Human Genome

Schones, Dustin E.; Cui, Kairong; Cuddapah, Suresh; Roh, Tae-Young; Barski, Artem; Wang, Zhibin; Wei, Gang; Zhao, Keji

doi:10.1016/j.cell.2008.02.022

Cited by 1,252 publications

(1,457 citation statements)

References 67 publications

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“…This is largely due to the requirement for chromatin to be reorganized to create access to key differentiation loci. The opening of chromatin is aided by the recruitment of histone acetyl transferases (HATs), chromatin remodelling enzymes and histone methyltransferases (HMTs), as well as the recently discovered histone lysine demethylases (KDMs) and ten-eleven translocation (TET; also known as methylcytosine dioxygenase) proteins that initiate DNA demethylation [130][131][132][133][134][135][136] (FIG. 5b).…”

Section: Dna Accessibility By Modification Of Dna and Histonesmentioning

confidence: 99%

Harnessing the plasticity of CD4+ T cells to treat immune-mediated disease

2016

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| CD4 + T cells differentiate and acquire distinct functions to combat specific pathogens but can also adapt their functions in response to changing circumstances. Although this phenotypic plasticity can be potentially deleterious, driving immune pathology, it also provides important benefits that have led to its evolutionary preservation. Here, we review CD4 + T cell plasticity by examining the molecular mechanisms that regulate it -from the extracellular cues that initiate and drive cells towards varying phenotypes, to the cytosolic signalling cascades that decipher these cues and transmit them into the cell and to the nucleus, where these signals imprint specific gene expression programmes. By understanding how this functional flexibility is achieved, we may open doors to new therapeutic approaches that harness this property of T cells.

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Section: Dna Accessibility By Modification Of Dna and Histonesmentioning

confidence: 99%

Harnessing the plasticity of CD4+ T cells to treat immune-mediated disease

2016

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“…NFRs have been mapped across genomes by mapping the nucleosome occupancy at high resolution. [27][28][29][30] Computational and experimental approaches can largely reconstitute patterns that are observed in cells, suggesting information encoded in the DNA itself plays a major role in directing nucleosome placement. Complete reconstitution of observed nucleosomal patterns is generally attributed to transcription factor-dependent recruitment of nucleosome remodeling complexes.…”

Section: Divergent Transcription In Yeastmentioning

confidence: 99%

Divergent transcription: A new feature of active promoters

Seila¹,

Core²,

Lis³

et al. 2009

Cell Cycle

169

164

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“…It has been reported that nucleosomes acquire an open chromatin structure following the binding of transcription factors ). To analyze the nucleosome structure, Nucleosome-Seq (Albert et al 2007;Jiang and Pugh 2009;Schones et al 2008) was used in DLD-1 and TIG-3 cells. We generated a total of 130,088,634 36-bp sequence tags from micrococcal nuclease-digested genomic DNA and calculated the occupancy of the nucleosome according to a previously reported procedure (Albert et al 2007) (Supplementary Fig.…”

Section: Epigenetic Regulation In Regions Surrounding Hif-1a Binding mentioning

confidence: 99%

“…Furthermore, we carried out Illumina GA sequencing analysis using micrococcal nuclease-digested genomic DNA (Nucleosome-Seq) (Albert et al 2007;Jiang and Pugh 2009;Schones et al 2008). We examined the changes in nucleosome structure caused by HIF-1a binding and the subsequent transcriptional activation.…”

Section: Introductionmentioning

confidence: 99%

Genome-wide identification and annotation of HIF-1α binding sites in two cell lines using massively parallel sequencing

Tanimoto

Tsuchihara

Kanai

et al. 2010

HUGO J

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We identified 531 and 616 putative HIF-1a target sites by ChIP-Seq in the cancerous cell line DLD-1 and the non-cancerous cell line TIG-3, respectively. We also examined the positions and expression levels of transcriptional start sites (TSSs) in these cell lines using our TSS-Seq method. We observed that 121 and 48 genes in DLD-1 and TIG-3 cells, respectively, had HIF-1a binding sites in proximal regions of the previously reported TSSs that were up-regulated at the transcriptional level. In addition, 193 and 123 of the HIF-1a target sites, respectively, were located in proximal regions of previously uncharacterized TSSs, namely, TSSs of putative alternative promoters of protein-coding genes or promoters of putative non-protein-coding transcripts. The hypoxic response of DLD-1 cells was more significant than that of TIG-3 cells with respect to both the number of target sites and the degree of induced changes in transcript expression. The Nucleosome-Seq and ChIP-Seq analyses of histone modifications revealed that the chromatin formed an open structure in regions surrounding the HIF-1a binding sites, but this event occurred prior to the actual binding of HIF1a. Different cellular histories may be encoded by chromatin structures and determine the activation of specific genes in response to hypoxic shock.

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Dynamic Regulation of Nucleosome Positioning in the Human Genome

Cited by 1,252 publications

References 67 publications

Harnessing the plasticity of CD4+ T cells to treat immune-mediated disease

Harnessing the plasticity of CD4+ T cells to treat immune-mediated disease

Divergent transcription: A new feature of active promoters

Genome-wide identification and annotation of HIF-1α binding sites in two cell lines using massively parallel sequencing

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