Similar Datasets
Project description:Increasing evidence suggests that transcriptional control and chromatin activities at large involve regulatory RNAs, which likely enlist specific RNA-binding proteins (RBPs). Although multiple RBPs have been implicated in transcription control, it has remained unclear how extensively RBPs directly act on chromatin. We embarked on a large-scale RBP ChIP-seq analysis, revealing widespread RBP presence in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also show strong preference for hotspots in the genome, particularly gene promoters, where their association is frequently linked to transcriptional output. Unsupervised clustering reveals extensive co-association between TFs and RBPs, as exemplified by YY1, a known RNA-dependent TF, and RBM25, an RBP involved in splicing regulation. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping, and transcription. We propose that various RBPs may enhance network interaction through harnessing regulatory RNAs to control transcription.
| S-EPMC6760001 | biostudies-literature
Project description:Increasing evidence suggests that transcriptional control and chromatin activities at large involve regulatory RNAs, which likely enlist specific RNA binding proteins (RBPs). Although multiple RBPs have been implicated in transcriptional control, it has remained unclear how extensively RBPs directly act on chromatin. We embarked on a large-scale RBP ChIP-seq analysis, revealing widespread RBP presence in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also showed strong preference for hotspots in the genome, particularly gene promoters, where their association is frequently linked to transcriptional output. Unsupervised clustering reveals extensive co-association between TFs and RBPs, as exemplified by YY1, a known RNA-dependent TF, and RBM25, an RBP involved in splicing regulation. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping and transcription. We propose that various RBPs may enhance network interaction through harnessing regulatory RNAs to control transcription. As part of the ENCODE consortium, we embarked on a large-scale RBP ChIP-seq analysis, revealing broad presence of RBPs in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also show great preference for hotspots in the genome, particularly gene promoters, where their binding is frequently linked to transcriptional output. Self-organizing map reveals extensive co-binding events between TFs and RBPs, as exemplified by those between YY1, a known RNA-dependent TF, and RBM25, an RBP involved in alternative splicing. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping and transcription. We propose that various RBPs may bridge specific TF-RNA interactions to control transcription.
2019-06-27 | GSE120105 | GEO
Project description:Increasing evidence suggests that transcriptional control and chromatin activities at large involve regulatory RNAs, which likely enlist specific RNA binding proteins (RBPs). Although multiple RBPs have been implicated in transcriptional control, it has remained unclear how extensively RBPs directly act on chromatin. We embarked on a large-scale RBP ChIP-seq analysis, revealing widespread RBP presence in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also showed strong preference for hotspots in the genome, particularly gene promoters, where their association is frequently linked to transcriptional output. Unsupervised clustering reveals extensive co-association between TFs and RBPs, as exemplified by YY1, a known RNA-dependent TF, and RBM25, an RBP involved in splicing regulation. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping and transcription. We propose that various RBPs may enhance network interaction through harnessing regulatory RNAs to control transcription.
2019-06-27 | GSE120104 | GEO
Project description:Increasing evidence suggests that transcriptional control and chromatin activities at large involve regulatory RNAs, which likely enlist specific RNA binding proteins (RBPs). Although multiple RBPs have been implicated in transcriptional control, it has remained unclear how extensively RBPs directly act on chromatin. We embarked on a large-scale RBP ChIP-seq analysis, revealing widespread RBP presence in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also showed strong preference for hotspots in the genome, particularly gene promoters, where their association is frequently linked to transcriptional output. Unsupervised clustering reveals extensive co-association between TFs and RBPs, as exemplified by YY1, a known RNA-dependent TF, and RBM25, an RBP involved in splicing regulation. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping and transcription. We propose that various RBPs may enhance network interaction through harnessing regulatory RNAs to control transcription.
2019-06-27 | GSE120023 | GEO
Project description:Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription
| PRJNA491670 | ENA
Project description:Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [HiC-Seq]
| PRJNA491667 | ENA
Project description:Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [ChIP-Seq]
| PRJNA491668 | ENA
Project description:Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [GRO-Seq]
| PRJNA491665 | ENA
Project description:Pervasive transcripts (PTs) are difficult to detect by steady-state RNA-seq, because they are degraded immediately by the nuclear exosome complex. Here, we describe a protocol illustrating a bioinformatic pipeline for genome-wide PTs de novo annotation via chromatin-associated RNA-seq data upon DIS3 depletion. Compared to defining PTs by nascent RNA-seq such as TT-seq and PRO-seq, this protocol is more convenient and cost efficient. In addition, this protocol defines 3'-end of PTs more precisely, while reads from PRO-seq have a skew at the 5'-end. For complete details on the use and execution of this protocol, please refer to Liu et al. (2022).
| S-EPMC9184797 | biostudies-literature
Project description:Transcription factors (TF) bind to chromatin and regulate the expression of genes. The pair Myc:Max binds to E-box regulatory DNA elements throughout the genome, controlling transcription of a large group of specific genes. We introduce an implicit modeling protocol for Myc:Max binding to mesoscale chromatin fibers to determine TF effect on chromatin architecture and shed light on its mechanism of gene regulation. We first bind Myc:Max to different chromatin locations and show how it can direct fiber folding and formation of microdomains, and how this depends on the linker DNA length. Second, by simulating increasing concentrations of Myc:Max binding to fibers that differ in the DNA linker length, linker histone density, and acetylation levels, we assess the interplay between Myc:Max and other chromatin internal parameters. Third, we study the mechanism of gene silencing by Myc:Max binding to the Eed gene loci. Overall, our results show how chromatin architecture can be regulated by TF binding. The position of TF binding dictates the formation of microdomains that appear visible only at the ensemble level. On the other hand, the presence of linker histone, acetylations, or different linker DNA lengths regulates the concentration-dependent effect of TF binding. Furthermore, we show how TF binding can repress gene expression by increasing fiber folding motifs that help compact and occlude the promoter region. Importantly, this effect can be reversed by increasing linker histone density. Overall, these results shed light on the epigenetic control of the genome dictated by TF binding.
| S-EPMC10557667 | biostudies-literature