Similar Datasets
Project description:Although the 3D genome architecture is essential for long-range gene regulation, the significance of physical chromatin interactions is challenged by recent findings of mutual insensitiveness between contact propensity and gene expression. Here we report hundred basepair-resolution profiling of chromatin conformation in 33 colon tissues tracing the formation and malignant transformation of colorectal polyps. We identified progressive genome-wide decays of chromatin structures such as interaction stripes and loops on all types of cis-regulatory elements, particularly promoters, independent to the alterations of DNA methylation and chromatin accessibility. Instead of linearly correlated with degree of structural decays, transcription levels shifted toward correction of their quantitative mismatching with corresponding promoter contact propensity. These observations suggest increasing sensitivity of transcription to regulatory architecture integrity along with its loss during early cancer development, a mechanism which may provide novel insights to the misregulations of cancer driving genes.
2022-08-29 | GSE207951 | GEO
Project description:Although the 3D genome architecture is essential for long-range gene regulation, the significance of physical chromatin interactions is challenged by recent findings of mutual insensitiveness between contact propensity and gene expression. Here we report hundred basepair-resolution profiling of chromatin conformation in 33 colon tissues tracing the formation and malignant transformation of colorectal polyps. We identified progressive genome-wide decays of chromatin structures such as interaction stripes and loops on all types of cis-regulatory elements, particularly promoters, independent to the alterations of DNA methylation and chromatin accessibility. Instead of linearly correlated with degree of structural decays, transcription levels shifted toward correction of their quantitative mismatching with corresponding promoter contact propensity. These observations suggest increasing sensitivity of transcription to regulatory architecture integrity along with its loss during early cancer development, a mechanism which may provide novel insights to the misregulations of cancer driving genes.
2022-08-29 | GSE207950 | GEO
Project description:Although the 3D genome architecture is essential for long-range gene regulation, the significance of physical chromatin interactions is challenged by recent findings of mutual insensitiveness between contact propensity and gene expression. Here we report hundred basepair-resolution profiling of chromatin conformation in 33 colon tissues tracing the formation and malignant transformation of colorectal polyps. We identified progressive genome-wide decays of chromatin structures such as interaction stripes and loops on all types of cis-regulatory elements, particularly promoters, independent to the alterations of DNA methylation and chromatin accessibility. Instead of linearly correlated with degree of structural decays, transcription levels shifted toward correction of their quantitative mismatching with corresponding promoter contact propensity. These observations suggest increasing sensitivity of transcription to regulatory architecture integrity along with its loss during early cancer development, a mechanism which may provide novel insights to the misregulations of cancer driving genes.
2022-08-29 | GSE207949 | GEO
Project description:Although the 3D genome architecture is essential for long-range gene regulation, the significance of physical chromatin interactions is challenged by recent findings of mutual insensitiveness between contact propensity and gene expression. Here we report hundred basepair-resolution profiling of chromatin conformation in 33 colon tissues tracing the formation and malignant transformation of colorectal polyps. We identified progressive genome-wide decays of chromatin structures such as interaction stripes and loops on all types of cis-regulatory elements, particularly promoters, independent to the alterations of DNA methylation and chromatin accessibility. Instead of linearly correlated with degree of structural decays, transcription levels shifted toward correction of their quantitative mismatching with corresponding promoter contact propensity. These observations suggest increasing sensitivity of transcription to regulatory architecture integrity along with its loss during early cancer development, a mechanism which may provide novel insights to the misregulations of cancer driving genes.
2024-02-11 | GSE255300 | GEO
Project description:BackgroundBread wheat (Triticum aestivum) is an allohexaploid that is generated by two subsequent allopolyploidization events. The large genome size (16 Gb) and polyploid complexity impede our understanding of how regulatory elements and their interactions shape chromatin structure and gene expression in wheat. The open chromatin enrichment and network Hi-C (OCEAN-C) is a powerful antibody-independent method to detect chromatin interactions between open chromatin regions throughout the genome.ResultsHere we generate open chromatin interaction maps for hexaploid wheat and its tetraploid and diploid relatives using OCEAN-C. The anchors of chromatin loops show high chromatin accessibility and are concomitant with several active histone modifications, with 67% of them interacting with multiple loci. Binding motifs of various transcription factors are significantly enriched in the hubs of open chromatin interactions (HOCIs). The genes linked by HOCIs represent higher expression level and lower coefficient expression variance than the genes linked by other loops, which suggests HOCIs may coordinate co-expression of linked genes. Thousands of interchromosomal loops are identified, while limited interchromosomal loops (0.4%) are identified between homoeologous genes in hexaploid wheat. Moreover, we find structure variations contribute to chromatin interaction divergence of homoeologs and chromatin topology changes between different wheat species. The genes with discrepant chromatin interactions show expression alteration in hexaploid wheat compared with its tetraploid and diploid relatives.ConclusionsOur results reveal open chromatin interactions in different wheat species, which provide new insights into the role of open chromatin interactions in gene expression during the evolution of polyploid wheat.
| S-EPMC8785527 | biostudies-literature
Project description:How the chromatin regulatory landscape in the inner cell mass cells is established from differentially packaged sperm and egg genomes during preimplantation development is unknown. Here, we develop a low-input DNase I sequencing (liDNase-seq) method that allows us to generate maps of DNase I-hypersensitive site (DHS) of mouse preimplantation embryos from 1-cell to morula stage. The DHS landscape is progressively established with a drastic increase at the 8-cell stage. Paternal chromatin accessibility is quickly reprogrammed after fertilization to the level similar to maternal chromatin, while imprinted genes exhibit allelic accessibility bias. We demonstrate that transcription factor Nfya contributes to zygotic genome activation and DHS formation at the 2-cell stage and that Oct4 contributes to the DHSs gained at the 8-cell stage. Our study reveals the dynamic chromatin regulatory landscape during early development and identifies key transcription factors important for DHS establishment in mammalian embryos.
| S-EPMC6625655 | biostudies-literature
Project description:Each Caulobacter cell cycle involves differentiation and an asymmetric cell division driven by a cyclical regulatory circuit comprised of four transcription factors (TFs) and a DNA methyltransferase. Using a modified global 5' RACE protocol, we globally mapped transcription start sites (TSSs) at base-pair resolution, measured their transcription levels at multiple times in the cell cycle, and identified their transcription factor binding sites. Out of 2726 TSSs, 586 were shown to be cell cycle-regulated and we identified 529 binding sites for the cell cycle master regulators. Twenty-three percent of the cell cycle-regulated promoters were found to be under the combinatorial control of two or more of the global regulators. Previously unknown features of the core cell cycle circuit were identified, including 107 antisense TSSs which exhibit cell cycle-control, and 241 genes with multiple TSSs whose transcription levels often exhibited different cell cycle timing. Cumulatively, this study uncovered novel new layers of transcriptional regulation mediating the bacterial cell cycle.
| S-EPMC4287350 | biostudies-literature
Project description:Myofibres (primary and secondary myofibre) are the basic structure of muscle and the determinant of muscle mass. To explore the skeletal muscle developmental processes from primary myofibres to secondary myofibres in pigs, we conducted an integrative three-dimensional structure of genome and transcriptomic characterization of longissimus dorsi muscle of pig from primary myofibre formation stage [embryonic Day 35 (E35)] to secondary myofibre formation stage (E80). In the hierarchical genomic structure, we found that 11.43% of genome switched compartment A/B status, 14.53% of topologically associating domains are changed intradomain interactions (D-scores) and 2,730 genes with differential promoter-enhancer interactions and (or) enhancer activity from E35 to E80. The alterations of genome architecture were found to correlate with expression of genes that play significant roles in neuromuscular junction, embryonic morphogenesis, skeletal muscle development or metabolism, typically, NEFL, MuSK, SLN, Mef2D and GCK. Significantly, Sox6 and MATN2 play important roles in the process of primary to secondary myofibres formation and increase the regulatory potential score and genes expression in it. In brief, we reveal the genomic reorganization from E35 to E80 and construct genome-wide high-resolution interaction maps that provide a resource for studying long-range control of gene expression from E35 to E80.
| S-EPMC8154859 | biostudies-literature
Project description:Congenital heart disease (CHD) affects eight out of 1,000 live births and is a major social and health-care burden. A common genetic cause of CHD is the 22q11.2 deletion, which is the basis of the homonymous deletion syndrome (22q11.2DS), also known as DiGeorge syndrome. Most of its clinical spectrum is caused by haploinsufficiency of Tbx1, a gene encoding a T-box transcription factor. Here we show that Tbx1 positively regulates monomethylation of histone 3 lysine 4 (H3K4me1) through interaction with and recruitment of histone methyltransferases. Treatment of cells with tranylcypromine (TCP), an inhibitor of histone demethylases, rebalances the loss of H3K4me1 and rescues the expression of approximately one-third of the genes dysregulated by Tbx1 suppression. In Tbx1 mouse mutants, TCP treatment ameliorates substantially the cardiovascular phenotype. These data suggest that epigenetic drugs may represent a potential therapeutic strategy for rescue of gene haploinsufficiency phenotypes, including structural defects.
| S-EPMC4895808 | biostudies-literature
Project description:In recent years, there has been a significant increase in the study of own and foreign human factors favoring the development of different types of cancer, including genetic and environmental ones. However, the fact that the immune response plays a fundamental role in the development of immunity and susceptibility to colorectal cancer (CRC) is much stronger. Among the many cell populations of the immune system that participate in restricting or favoring CRC development, regulatory T cells (Treg) play a major role in orchestrating immunomodulation during CRC. In this review, we established concrete evidence supporting the fact that Treg cells have an important role in the promotion of tumor development during CRC, mediating an increasing suppressive capacity which controls the effector immune response, and generating protection for tumors. Furthermore, Treg cells go through a process called "phenotypic plasticity", where they co-express transcription factors that promote an inflammatory profile. We reunited evidence that describes the interaction between the different effector populations of the immune response and its modulation by Treg cells adapted to the tumor microenvironment, including the mechanisms used by Treg cells to suppress the protective immune response, as well as the different subpopulations of Treg cells participating in tumor progression, generating susceptibility during CRC development. Finally, we discussed whether Treg cells might or might not be a therapeutic target for an effective reduction in the morbidity and mortality caused by CRC.
| S-EPMC7409056 | biostudies-literature