A Genome Scale Location Analysis of Human Staf/ZNF143-binding Sites Suggests a Widespread Role for Human Staf/ZNF143 in Mammalian Promoters

Myslinski, Evelyne; Gérard, Marie-Aline; Krol, Alain; Carbon, Philippe

doi:10.1074/jbc.m608507200

Cited by 57 publications

(85 citation statements)

References 30 publications

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“…ZNF143 is a ubiquitously expressed zinc finger protein of unknown function originally identified as a regulator of selenomethionine tRNA gene expression (35). Our ChIP-Seq analyses confirm prior studies suggesting that ZNF143 localizes to promoters (36), particularly those driving transcription bidirectionally (17). Gene pairs regulated by bidirectional promoters are highly conserved in vertebrates (37); whether this is a consequence of convergent functions necessitating coordinate regulation or chance insertion of a coding sequence adjacent to a promoter with bidirectional activity during early vertebrate evolution is uncertain.…”

Section: Discussionsupporting

confidence: 84%

Genome-wide analysis reveals conserved and divergent features of Notch1/RBPJ binding in human and murine T-lymphoblastic leukemia cells

Wang¹,

Zou

Zhao

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

229

227

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Notch1 regulates gene expression by associating with the DNA-binding factor RBPJ and is oncogenic in murine and human T-cell progenitors. Using ChIP-Seq, we find that in human and murine T-lymphoblastic leukemia (TLL) genomes Notch1 binds preferentially to promoters, to RBPJ binding sites, and near imputed ZNF143, ETS, and RUNX sites. ChIP-Seq confirmed that ZNF143 binds to ∼40% of Notch1 sites. Notch1/ZNF143 sites are characterized by high Notch1 and ZNF143 signals, frequent cobinding of RBPJ (generally through sites embedded within ZNF143 motifs), strong promoter bias, and relatively low mean levels of activating chromatin marks. RBPJ and ZNF143 binding to DNA is mutually exclusive in vitro, suggesting RBPJ/Notch1 and ZNF143 complexes exchange on these sites in cells. K-means clustering of Notch1 binding sites and associated motifs identified conserved Notch1-RUNX, Notch1-ETS, Notch1-RBPJ, Notch1-ZNF143, and Notch1-ZNF143-ETS clusters with different genomic distributions and levels of chromatin marks. Although Notch1 binds mainly to gene promoters, ∼75% of direct target genes lack promoter binding and are presumably regulated by enhancers, which were identified near MYC , DTX1 , IGF1R , IL7R , and the GIMAP cluster. Human and murine TLL genomes also have many sites that bind only RBPJ. Murine RBPJ-only sites are highly enriched for imputed REST (a DNA-binding transcriptional repressor) sites, whereas human RPBJ-only sites lack REST motifs and are more highly enriched for imputed CREB sites. Thus, there is a conserved network of cis -regulatory factors that interacts with Notch1 to regulate gene expression in TLL cells, as well as unique classes of divergent RBPJ-only sites that also likely regulate transcription.

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Section: Discussionsupporting

confidence: 84%

Genome-wide analysis reveals conserved and divergent features of Notch1/RBPJ binding in human and murine T-lymphoblastic leukemia cells

Wang¹,

Zou

Zhao

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

229

227

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“…4A, hStaf was easily detected in anti-CHD8 immunoprecipitates, and CHD8 was detected, albeit weakly, in anti-hStaf immunoprecipitates (lanes 3 and 6), suggesting that CHD8 and hStaf interact inside cells. However, since hStaf is involved in transcription activation of several Pol II and Pol III genes (34,50), it was possible that hStaf interacted with CHD8 but did not recruit CHD8 to the U6 promoter. We therefore tested whether CHD8 is localized on the U6 promoter by ChIP as described above.…”

Section: Results Hstaf Activates U6 Transcription From a Chromatin Tementioning

confidence: 99%

CHD8 Associates with Human Staf and Contributes to Efficient U6 RNA Polymerase III Transcription

Yuan

Zhao

Florens

et al. 2007

Molecular and Cellular Biology

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Chromatin remodeling and histone modification are essential for eukaryotic transcription regulation, but little is known about chromatin-modifying activities acting on RNA polymerase III (Pol III)-transcribed genes. The human U6 small nuclear RNA promoter, located 5 of the transcription start site, consists of a core region directing basal transcription and an activating region that recruits the transcription factors Oct-1 and Staf (ZNF143). Oct-1 activates transcription in part by helping recruit core binding factors, but nothing is known about the mechanisms of transcription activation by Staf. We show that Staf activates U6 transcription from a preassembled chromatin template in vitro and associates with several proteins linked to chromatin modification, among them chromodomain-helicase-DNA binding protein 8 (CHD8). CHD8 binds to histone H3 diand trimethylated on lysine 4. It resides on the human U6 promoter as well as the mRNA IRF3 promoter in vivo and contributes to efficient transcription from both these promoters. Thus, Pol III transcription from type 3 promoters uses some of the same factors used for chromatin remodeling at Pol II promoters.The state of chromatin packaging defines in large part the transcriptional competency of genes transcribed by RNA polymerases (Pol) I and II. In this process, it is clear that the packaging of DNA into certain chromatin states has a repressive effect on transcription, in particular on the initiation and elongation steps, as histone octamers within nucleosomes can block the binding of transcription initiation factors and hamper the progress of RNA Pol along a gene (24,40,48,79). For transcription to take place, the chromatin template needs to be modified such that the accessibility of transcription factors to their promoter targets is increased and transcription elongation is facilitated (36,74).Chromatin modification at Pol II genes is accomplished by a large number of factors (47) that are recruited to chromatin through contacts with (i) histones with various modifications in their N-terminal regions, (ii) the DNA, and (iii) certain activators. Such activators can bind to chromatin templates and recruit chromatin-modifying factors, which then remodel nucleosomes or modify histones (11, 23). Successive waves of chromatin modifications are thought to allow for the regulated assembly of transcription initiation complexes, leading to active transcription.Much less is known about the requirements for chromatin modification at Pol III-transcribed genes. Pol III, like Sp6 Pol, is capable of transcribing through a nucleosome on a mononucleosomal template, causing an intranucleosomal loop followed by transfer of the histone octamer to a different position of the same template (62,63). This shows that Pol III can transcribe through a single nucleosome without the help of chromatin-modifying activities. However, a large number of observations suggests that the initiation step of Pol III transcription, as well as elongation through more than a single nucleosome, is influenced by...

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“…S6). ZNF143-ext (Myslinski et al 2006) and CTCF-ext (Ohlsson et al 2001;Rhee and Pugh 2011) have been documented before. GATA1-ext is the motif for the TAL-GATA1 complex (Xu et al 2003).…”

Section: Previously Unannotated Motifsmentioning

confidence: 90%

Sequence features and chromatin structure around the genomic regions bound by 119 human transcription factors

et al. 2012

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Chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) has become the dominant technique for mapping transcription factor (TF) binding regions genome-wide. We performed an integrative analysis centered around 457 ChIP-seq data sets on 119 human TFs generated by the ENCODE Consortium. We identified highly enriched sequence motifs in most data sets, revealing new motifs and validating known ones. The motif sites (TF binding sites) are highly conserved evolutionarily and show distinct footprints upon DNase I digestion. We frequently detected secondary motifs in addition to the canonical motifs of the TFs, indicating tethered binding and cobinding between multiple TFs. We observed significant position and orientation preferences between many cobinding TFs. Genes specifically expressed in a cell line are often associated with a greater occurrence of nearby TF binding in that cell line. We observed cell-linespecific secondary motifs that mediate the binding of the histone deacetylase HDAC2 and the enhancer-binding protein EP300. TF binding sites are located in GC-rich, nucleosome-depleted, and DNase I sensitive regions, flanked by wellpositioned nucleosomes, and many of these features show cell type specificity. The GC-richness may be beneficial for regulating TF binding because, when unoccupied by a TF, these regions are occupied by nucleosomes in vivo. We present the results of our analysis in a TF-centric web repository Factorbook (http://factorbook.org) and will continually update this repository as more ENCODE data are generated.

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A Genome Scale Location Analysis of Human Staf/ZNF143-binding Sites Suggests a Widespread Role for Human Staf/ZNF143 in Mammalian Promoters

Cited by 57 publications

References 30 publications

Genome-wide analysis reveals conserved and divergent features of Notch1/RBPJ binding in human and murine T-lymphoblastic leukemia cells

Genome-wide analysis reveals conserved and divergent features of Notch1/RBPJ binding in human and murine T-lymphoblastic leukemia cells

CHD8 Associates with Human Staf and Contributes to Efficient U6 RNA Polymerase III Transcription

Sequence features and chromatin structure around the genomic regions bound by 119 human transcription factors

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