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Combinatorial patterning of chromatin regulators uncovered by genome-wide location analysis in human cells

ABSTRACT: Hundreds of Chromatin Regulators (CRs) control chromatin structure and function by catalyzing and binding histone modifications, yet the rules governing these key processes remain obscure. Here, we present a systematic approach to infer CR function. We developed ChIP-string, a meso-scale assay that combines chromatin immunoprecipitation with a signature readout of 487 representative loci. We applied ChIP-string to screen 145 antibodies, thereby identifying effective reagents, which we used to map the genome-wide binding of 29 CRs in two cell types. We found that specific combinations of CRs co-localize in characteristic patterns at distinct chromatin environments, genes of coherent functions and distal regulatory elements. When comparing between cell types, CRs redistribute to different loci, but maintain their modular and combinatorial associations. Our work provides a multiplex method that substantially enhances the ability to monitor CR binding, presents a large resource of CR maps, and reveals common principles for combinatorial CR function. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

ORGANISM(S): Homo sapiens

PROVIDER: GSE32509 | GEO | 2011/12/23

REPOSITORIES: GEO

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Combinatorial patterning of chromatin regulators uncovered by genome-wide location analysis in human cells

Project description:Hundreds of Chromatin Regulators (CRs) control chromatin structure and function by catalyzing and binding histone modifications, yet the rules governing these key processes remain obscure. Here, we present a systematic approach to infer CR function. We developed ChIP-string, a meso-scale assay that combines chromatin immunoprecipitation with a signature readout of 487 representative loci. We applied ChIP-string to screen 145 antibodies, thereby identifying effective reagents, which we used to map the genome-wide binding of 29 CRs in two cell types. We found that specific combinations of CRs co-localize in characteristic patterns at distinct chromatin environments, genes of coherent functions and distal regulatory elements. When comparing between cell types, CRs redistribute to different loci, but maintain their modular and combinatorial associations. Our work provides a multiplex method that substantially enhances the ability to monitor CR binding, presents a large resource of CR maps, and reveals common principles for combinatorial CR function. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Study of genom-wide binding of 29 CRs in two cell types.

2011-12-23 | E-GEOD-32509 | biostudies-arrayexpress

Partitioned Usage of Chromatin Remodelers by Nucleosome Displacing Factors

Project description:Nucleosome-displacing factors (NDFs) in yeast, similar to pioneer factors in higher eukaryotes, cause opening of closed chromatin and formation of nucleosome-depleted regions (NDRs). NDRs in yeast are also affected by ATP-dependent chromatin remodelers (CRs). However, how NDFs and CRs coordinate in nucleosome invasion and NDR formation is still unclear. Here, we designed a high-throughput method to systematically study the interplay between NDFs and CRs. By combining integrated synthetic oligonucleotide library with DNA methyltransferase-based, single-molecule nucleosome mapping, we measured the impact of CRs on NDRs generated by individual NDFs. We found that CRs were dispensable for nucleosome invasion by NDFs, and they function downstream of NDF binding to modulate the NDR length. A few CRs show high specificity towards certain NDFs; however, in most cases, CRs are recruited in a factor-nonspecific and length-dependent manner. Overall, our study represents a novel framework to investigate how NDFs and CRs cooperate to generate desired pattern of chromatin opening.

2022-04-06 | GSE199812 | GEO

Ten-eleven translocation proteins modulate the response to environmental stress in mice

Project description:5-hydroxymethylcytosine (5hmC) is enriched in brain and has been recognized as an important DNA modification. However, the roles of 5hmC and its “writers”, Ten-eleven translocation (Tet) proteins, in stress-induced response have yet to be elucidated. Here, we show that chronic restraint stress (CRS) induced the depression-like behavior in mice and resulted in a 5hmC reduction in prefrontal cortex (PFC). Interestingly, we found that the loss of Tet1 (Tet1 KO) led to the resistance to CRS while the loss of Tet2 (Tet2 KO) increased the susceptibility of mice to CRS. Genome-wide 5hmC profiling identified the phenotype associated stress-induced dynamically hydroxymethylated loci (PA-SI-DhML), which are strongly enriched with hypoxia-induced factor (HIF) binding motifs. We demonstrated the physical interaction between TET1 and HIF1α induced by CRS, and revealed that the increased HIF1α binding under CRS is associated with SI-DhML. These results together suggest that TET1 could regulate stress-induced response by interacting with HIF1α.

2018-11-21 | GSE106220 | GEO

Repurposing of the multiciliation gene regulatory network in fate specification of Cajal-Retzius neurons

Project description:Cajal-Retzius (CR) neurons are key players of cortical development that display a very unique transcriptomic identity. However, little is known about the mechanisms involved in their fate specification. Here we use scRNAseq to reconstruct the differentiation trajectory of hem-derived CR cells (CRs) and unravel the transient expression of a complete gene module previously known to control the cellular process of multiciliogenesis. However, we find that CRs do not undergo centriole amplification or multiciliation. We show that upon genetic disruption of Gmnc, the master regulator of the multiciliation cascade, CRs are initially produced but fail to reach their normal identity and lean towards an aberrant fate resulting in their massive apoptosis. We further dissect the contribution of multiciliation effector genes and identify Trp73 as a key determinant. Finally, we use in utero electroporation to demonstrate that the intrinsic competence of hem progenitors as well as the heterochronic expression of Gmnc prevent centriole amplification in the CR lineage. Our work exemplifies how the co-option of a complete gene module, repurposed to control a completely distinct process, may contribute to the emergence of novel cell identities.

2023-06-01 | GSE220237 | GEO

Distinct functions of three chromatin remodelers in activator binding and preinitiation complex assembly

Project description:ATP-dependent chromatin remodelers (CRs), including SWI/SNF, RSC and Ino80C in budding yeast, are thought to stimulate transcription by repositioning or evicting promoter nucleosomes. The relative importance of these CRs in stimulating activator binding and recruitment of TATA-binding protein (TBP) to promoters is incompletely understood. Examining mutants depleted of the catalytic subunits of these CRs, we determined that RSC and Ino80C stimulate binding of transcription factor Gcn4 to nucleosome-depleted regions, or linkers between genic nucleosomes, at multiple target genes activated by Gcn4 in amino acid-starved cells, frequently by evicting nucleosomes from the Gcn4 binding motifs. At some genes, SWI/SNF functionally complements RSC, while opposing RSC at others to limit Gcn4 binding. The CRs in turn are recruited by Gcn4 to establish positive or negative feedback loops that control Gcn4 binding. The three CRs also cooperate to enhance TBP recruitment, again involving nucleosome depletion, at both Gcn4 target genes and highly expressed ribosomal protein genes, whereas only RSC and Ino80C act broadly throughout the genome to enhance this key step in preinitiation complex assembly. Our findings illuminate functional cooperation among multiple CRs in regulating activator binding and promoter activation.

2021-12-29 | GSE192592 | GEO

Hexavalent chromium disrupts chromatin organization and accessibility to CTCF sites in promoters of differentially expressed genes [MNase-Seq]

Project description:Hexavalent chromium compounds are well-established respiratory carcinogens utilized in industrial processes. While inhalation exposure constitutes an occupational risk affecting mostly chromium workers, environmental exposure from drinking water is a widespread gastrointestinal carcinogen, affecting millions of people throughout the world. Cr(VI) is genotoxic, by forming protein-Cr-DNA adducts and silencing tumor suppressor genes, but its mechanism of action at the molecular level is poorly understood. We have used FAIRE to show that Cr(VI) elicits broad changes in chromatin accessibility resulting from disruption of the binding of transcription factors CTCF and AP-1 to their cognate sites in chromatin. Here, we have used two complementary approaches to test the hypothesis that chromium perturbs chromatin organization and dynamics. DANPOS2 analyses of MNase.seq data identified several chromatin alterations induced by Cr(VI) affecting nucleosome architecture, including occupancy changes at specific genome locations; position shifts of 10 nucleotides or more; and fuzziness, or changes in signal amplitude. Using ATAC to analyze changes in chromatin accessibility, we found that Cr(VI) opened differentially accessible chromatin domains in a dose-dependent manner. These domains were enriched for the previously identified binding motifs for CTCF and AP-1, many located in promoters of differentially expressed genes. Cr(VI)-enriched CTCF sites were confirmed by ChIP.seq and, when compared with ENCODE-validated CTCF site datasets from mouse liver, correlated with evolutionarily conserved similar sites occupied in vivo. Our results show that Cr(VI) exposure promotes broad changes in chromatin accessibility and suggest that the subsequent dysregulation of transcription may result from the disruption of CTCF binding and nucleosome spacing, suggesting that transcription regulatory mechanisms are primary Cr(VI) targets.

2018-01-01 | GSE104565 | GEO

Hexavalent chromium disrupts chromatin organization and accessibility to CTCF sites in promoters of differentially expressed genes [ChIP-seq]

2018-01-01 | GSE104564 | GEO

Hexavalent chromium disrupts chromatin organization and accessibility to CTCF sites in promoters of differentially expressed genes [ATAC-seq]

2018-01-01 | GSE104563 | GEO

Cr(VI) Promotes Differential Binding of CTCF to its Cognate Sites

Project description:Using ChIP-seq, we characterize the differential binding of CTCF following 48 hours of low-dose, Cr(VI) treatment. Differentially-bound sites are enriched in regions near genes that are actively transcribed in the basal state and strength of initial binding may be a factor in determining the directionality of binding affinity fluctuations. CTCF and cohesin samples were used to predict intra-TAD chromatin loops in an effort to provide an initial characterization of how Cr(VI) potentially disrupts chromatin-chromatin contacts important for the regulation of transcription, serving as a foundation for future studies.

2020-07-21 | GSE154387 | GEO

Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) Analysis Uncovers Broad Changes in Chromatin Structure Resulting from Hexavalent Chromium Exposure

Project description:The ability of chromatin to switch back and forth from open euchromatin to closed heterochromatin is vital for transcriptional regulation and genomic stability, and subject to disruption by exposure to environmental agents such as hexavalent chromium. Cr(VI) exposure can cause chromosomal disruption through formation of Cr-DNA adducts, free radical-induced DNA damage, and DNA-Cr-protein and DNA-Cr-DNA cross-links, all of which may disrupt chromatin remodeling mechanisms responsible for maintenance or controlled modification of epigenetic homeostasis. In addition, dose-response analyses have shown that acute exposures to high-concentrations of Cr(VI) and chronic exposures to low-concentrations of the same agent lead to significantly different transcriptomic and genomic stability outcomes. To investigate how transcriptional responses to chromium exposure might correlate to structural changes in chromatin, we have used whole genome Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) analysis coupled with deep sequencing to identify regions of the genome that switch from open to closed chromatin or vice versa in response to exposure to varying Cr(VI) concentrations. We find that the switch affects gene expression levels in the target areas that vary depending on Cr(VI) concentration. At either Cr(VI) concentration, chromatin domains surrounding binding sites for AP-1 transcription factors become significantly open, treatment whereas BACH2 and CTCF binding sites are open solely at the low and high concentrations, respectively. Our results suggest that FAIRE may be a useful technique to map chromatin elements targeted by DNA damaging agents for which there is no prior knowledge of their specificity, and to identify subsequent transcriptomic changes induced by those agents.

2014-04-10 | GSE56636 | GEO

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