Similar Datasets
Project description:we report that regional expression of the Hoxc genes is regulated by antagonistic switch between repression and activation epigenetic modification. In freshly isolated dermal cells from P50 telogen Wt/Wt ear skin, no enrichment of H3K27ac was detected at Hoxc cluster, consistent with their lack of expression; in contrast, robust peaks of this marker are observed in 3’ region of the Hoxc cluster in dorsal skin dermal cells. Secondly we looked at H3K27 trimethylation (H3K27me3), a marker for polycomb-dependent gene repression, which antagonizes H3K27ac. Concomitantly, we found that H3K27me3 spread across the entire Hoxc cluster in adult ear skin dermal cells but was restricted to the 5’ region of the Hoxc cluster in adult dorsal skin dermal cells . In adult dorsal skin dermal cells, we found three occupied CTCF binding sites inside Hoxc cluster. The rostral CTCF binding site marks the discontinuity point of H3K27me3 modification at the intergenic region between Hoxc11 and Hoxc10 in dorsal skin dermal cells. This indicates the CTCF binding event within Hoxc cluster might forge a topological barrier that can insulate activation region from repression region and therefore lead to the region specific expression of the Hoxc cluster genes.To directly test whether there is ectopic interaction between Hoxc cluster and the active domain in proximal-TAD, we used circularized chromosome conformation capture (4C) with Hoxc4 as bait. In Wt/Koa ear skin dermal cells, there are clear ectopic interactions of Hoxc4 with the remaining active regulatory landscape in proximal-TAD; on the other hand, all of the interactions of Hoxc4 remained inside the distal-TAD with repressive domain in Wt/Wt ear skin.
2018-07-09 | GSE116720 | GEO
Project description:we report that regional expression of the Hoxc genes is regulated by antagonistic switch between repression and activation epigenetic modification. In freshly isolated dermal cells from P50 telogen Wt/Wt ear skin, no enrichment of H3K27ac was detected at Hoxc cluster, consistent with their lack of expression; in contrast, robust peaks of this marker are observed in 3’ region of the Hoxc cluster in dorsal skin dermal cells. Secondly we looked at H3K27 trimethylation (H3K27me3), a marker for polycomb-dependent gene repression, which antagonizes H3K27ac. Concomitantly, we found that H3K27me3 spread across the entire Hoxc cluster in adult ear skin dermal cells but was restricted to the 5’ region of the Hoxc cluster in adult dorsal skin dermal cells . In adult dorsal skin dermal cells, we found three occupied CTCF binding sites inside Hoxc cluster. The rostral CTCF binding site marks the discontinuity point of H3K27me3 modification at the intergenic region between Hoxc11 and Hoxc10 in dorsal skin dermal cells. This indicates the CTCF binding event within Hoxc cluster might forge a topological barrier that can insulate activation region from repression region and therefore lead to the region specific expression of the Hoxc cluster genes.To directly test whether there is ectopic interaction between Hoxc cluster and the active domain in proximal-TAD, we used circularized chromosome conformation capture (4C) with Hoxc4 as bait. In Wt/Koa ear skin dermal cells, there are clear ectopic interactions of Hoxc4 with the remaining active regulatory landscape in proximal-TAD; on the other hand, all of the interactions of Hoxc4 remained inside the distal-TAD with repressive domain in Wt/Wt ear skin.
2018-07-09 | GSE116722 | GEO
Project description:we report that regional expression of the Hoxc genes is regulated by antagonistic switch between repression and activation epigenetic modification. In freshly isolated dermal cells from P50 telogen Wt/Wt ear skin, no enrichment of H3K27ac was detected at Hoxc cluster, consistent with their lack of expression; in contrast, robust peaks of this marker are observed in 3’ region of the Hoxc cluster in dorsal skin dermal cells. Secondly we looked at H3K27 trimethylation (H3K27me3), a marker for polycomb-dependent gene repression, which antagonizes H3K27ac. Concomitantly, we found that H3K27me3 spread across the entire Hoxc cluster in adult ear skin dermal cells but was restricted to the 5’ region of the Hoxc cluster in adult dorsal skin dermal cells . In adult dorsal skin dermal cells, we found three occupied CTCF binding sites inside Hoxc cluster. The rostral CTCF binding site marks the discontinuity point of H3K27me3 modification at the intergenic region between Hoxc11 and Hoxc10 in dorsal skin dermal cells. This indicates the CTCF binding event within Hoxc cluster might forge a topological barrier that can insulate activation region from repression region and therefore lead to the region specific expression of the Hoxc cluster genes.To directly test whether there is ectopic interaction between Hoxc cluster and the active domain in proximal-TAD, we used circularized chromosome conformation capture (4C) with Hoxc4 as bait. In Wt/Koa ear skin dermal cells, there are clear ectopic interactions of Hoxc4 with the remaining active regulatory landscape in proximal-TAD; on the other hand, all of the interactions of Hoxc4 remained inside the distal-TAD with repressive domain in Wt/Wt ear skin.
2018-07-09 | GSE116721 | GEO
Project description:Gene expression, epigenetic modification, and chromatin landscape of skin dermal cells in different body positions
| PRJNA479983 | ENA
Project description:Gene expression, epigenetic modification, and chromatin landscape of skin dermal cells in different body positions [4C]
| PRJNA479995 | ENA
Project description:Gene expression, epigenetic modification, and chromatin landscape of skin dermal cells in different body positions [RNA-Seq]
| PRJNA479996 | ENA
Project description:Gene expression, epigenetic modification, and chromatin landscape of skin dermal cells in different body positions [ChIP-Seq]
| PRJNA479997 | ENA
Project description:Proper regulation of the chromatin landscape is essential for maintaining eukaryotic cell identity and diverse cellular processes. The importance of the epigenome comes, in part, from the ability to influence gene expression through patterns in DNA methylation, histone tail modification, and chromatin architecture. Decades of research have associated this process of chromatin regulation and gene expression with human diseased states. With the goal of understanding how chromatin dysregulation contributes to disease, as well as preventing or reversing this type of dysregulation, a multidisciplinary effort has been launched to control the epigenome. Chemicals that alter the epigenome have been used in labs and in clinics since the 1970s, but more recently there has been a shift in this effort towards manipulating the chromatin landscape in a locus-specific manner. This review will provide an overview of chromatin biology to set the stage for the type of control being discussed, evaluate the recent technological advances made in controlling specific regions of chromatin, and consider the translational applications of these works.
| S-EPMC7038174 | biostudies-literature
Project description:The small ubiquitin-like modifier 2 (SUMO-2) is required for survival when cells are exposed to treatments that induce proteotoxic stress by causing the accumulation of misfolded proteins. Exposure of cells to heat shock or other forms of proteotoxic stress induces the conjugation of SUMO-2 to proteins in the nucleus. We investigated the chromatin landscape of SUMO-2 modifications in response to heat stress. Through chromatin immunoprecipitation assays coupled to high-throughput DNA sequencing and mRNA sequencing, we showed that in response to heat shock, SUMO-2 accumulated at nucleosome-depleted, active DNA regulatory elements, which represented binding sites for large protein complexes and were predominantly associated with active genes. However, SUMO did not act as a direct transcriptional repressor or activator of these genes during heat shock. Instead, integration of our results with published proteomics data on heat shock-induced SUMO-2 substrates supports a model in which the conjugation of SUMO-2 to proteins acts as an acute stress response that is required for the stability of protein complexes involved in gene expression and posttranscriptional modification of mRNA. We showed that the conjugation of SUMO-2 to chromatin-associated proteins is an integral component of the proteotoxic stress response, and propose that SUMO-2 fulfills its essential role in cell survival by contributing to the maintenance of protein complex homeostasis.
| S-EPMC6707813 | biostudies-literature
Project description:The organization of eukaryotic chromosomes into transcriptionally active euchromatin and repressed heterochromatin requires mechanisms that establish, maintain and distinguish these canonical chromatin domains. Post-translational modifications are fundamental in these processes. Monoubiquitylation of histones was discovered more than three decades ago, but its precise function has been enigmatic until recently. It is now appreciated that the spectrum of chromatin ubiquitylation is not restricted to monoubiquitylation of histones, but includes degradatory ubiquitylation of histones, histone-modifying enzymes and non-histone chromatin factors. These occur in a spatially and temporally controlled manner. In this review, we summarize our understanding of these mechanisms with a particular emphasis on how ubiquitylation shapes the physical landscape of chromatin.
| S-EPMC3388787 | biostudies-other