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3秒自动关闭窗口Promoter-distal RNA polymerase II binding discriminates active from inactive CCAAT/ enhancer-binding protein beta binding sites.
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):. doi: 10.1101/gr.. Epub
2015 Oct 20.Promoter-distal RNA polymerase II binding discriminates active from inactive CCAAT/ enhancer-binding protein beta binding sites.1, 1, 2, 1, 3, 3, 1, 2, 1.1HudsonAlpha Institute for Biotechnology, Huntsville, Alabama 35806, USA;2Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA;3Washington University at St. Louis, Center for Genome Sciences and Systems Biology, Department of Genetics, Washington University School of Medicine, St. Louis, Missouri 63108, USA.AbstractTranscription factors (TFs) bind to thousands of DNA sequences in mammalian genomes, but most of these binding events appear to have no direct effect on gene expression. It is unclear why only a subset of TF bound sites are actively involved in transcriptional regulation. Moreover, the key genomic features that accurately discriminate between active and inactive TF binding events remain ambiguous. Recent studies have identified promoter-distal RNA polymerase II (RNAP2) binding at enhancer elements, suggesting that these interactions may serve as a marker for active regulatory sequences. Despite these correlative analyses, a thorough functional validation of these genomic co-occupancies is still lacking. To characterize the gene regulatory activity of DNA sequences underlying promoter-distal TF binding events that co-occur with RNAP2 and TF sites devoid of RNAP2 occupancy using a functional reporter assay, we performed cis-regulatory element sequencing (CRE-seq). We tested more than 1000 promoter-distal CCAAT/enhancer-binding protein beta (CEBPB)-bound sites in HepG2 and K562 cells, and found that CEBPB-bound sites co-occurring with RNAP2 were more likely to exhibit enhancer activity. CEBPB-bound sites further maintained substantial cell-type specificity, indicating that local DNA sequence can accurately convey cell-type-specific regulatory information. By comparing our CRE-seq results to a comprehensive set of genome annotations, we identified a variety of genomic features that are strong predictors of regulatory element activity and cell-type-specific activity. Collectively, our functional assay results indicate that RNAP2 occupancy can be used as a key genomic marker that can distinguish active from inactive TF bound sites. (C) 2015 Savic et al.; Published by Cold Spring Harbor Laboratory Press.PMID:
[PubMed - in process] CRE-seq of CEBPB binding sites. Analysis of H3K4me1 (in purple) and H3K4me3 (in red) enrichment at CEBPB binding sites &5 kb from promoters (A) and &5 kb from promoters (B). Average ChIP-seq signal enrichment is displayed on the y-axis, whereas the distance from transcription start site (TSS) is displayed on the x-axis. At &5 kb from promoters, a substantial enrichment in H3K4me1 is observed. (C) Schematic of CRE-seq experimental platform. Oligonucleotides are generated harboring 120 bp of sequence centered on CEBPB binding site summits, unique 9-bp barcodes, and restriction enzyme sites for cloning. Oligonucleotides are cloned into a plasmid backbone, upstream of the backbone poly-A sequence, while a minimal promoter and luciferase coding sequence is subsequently cloned in between binding sites and barcodes within oligonucleotides, generating a pool of approximately 12,000 unique plasmids. HepG2 and K562 cells are transfected, in replicates, into HepG2 and K562 cells. DNA and RNA (cDNA) is extracted, barcodes from plasmids (DNA) and transcribed RNA molecules are amplified and prepared for next-generation sequencing. Regulatory activity for each barcode is determined by normalizing the RNA-derived barcode counts with counts from DNA (plasmids). The median activity across all barcodes for an individual element was used to determine activity in each replicate experiment. The mean activity across replicate experiments for each element was used to calculate the final activity. (D,E) Luciferase assay results in HepG2 (D) and K562 (E) cells are also displayed. The log2-transformed activity using luciferase assay (y-axis) and CRE-seq assay (x-axis) is shown (where fc denotes fold change). The Rank correlation for each data set is shown at the bottom right of each graph.Genome Res. ):.RNAP2-associated sites exhibit stronger activity. (A) Density plots of HepG2-specific CEBPB binding sequence activity in HepG2 cells. The x-axis displays the distribution of log2-transformed regulatory activity (RNA/DNA barcode counts), while the y-axis displays the density across distinct regulatory activities. HepG2 binding site CRE-seq activity distributions are shown in blue and compared with associated scrambled control sequence activities (shown in gray). (B) Density plots of K562-specific CEBPB binding sequence activity in K562 cells. The x-axis displays the distribution of log2-transformed regulatory activity (RNA/DNA barcode counts), while the y-axis displays the density across distinct regulatory activities. K562 binding site CRE-seq activity distributions are shown in red and compared with associated scrambled control sequence activities (shown in gray). (C) HepG2 CRE-seq activity for distinct classes of binding sites is shown as box plots. The log2-transformed CRE-seq activity (RNA/DNA barcode counts) is displayed on the y-axis. Binding sites that are coincident with promoter-distal RNAP2 are shown in dark blue, and the scrambled control sequences for these RNAP2-associated binding sites are displayed in dark gray. HepG2 binding sites devoid of promoter-distal RNAP2 binding are displayed in light blue, and the scrambled control sequences for these RNAP2-devoid sites are shown in light gray. The percentage of RNAP2-associated and RNAP2-devoid HepG2 sites above the 95th percentile of associated scrambled control sites are displayed on the plot. (D) K562 CRE-seq activity for distinct classes of binding sites is shown as box plots. The log2-transformed CRE-seq activity (RNA/DNA barcode counts) is displayed on the y-axis. Binding sites that are coincident with promoter-distal RNAP2 are shown in dark red, and the scrambled control sequences for these RNAP2-associated binding sites are displayed in dark gray. K562 binding sites devoid of promoter-distal RNAP2 binding are displayed in light red, and the scrambled control sequences for these RNAP2-devoid sites are shown in light gray. The percentage of RNAP2-associated and RNAP2-devoid K562 sites above the 95th percentile of associated scrambled control sites are displayed on the plot.Genome Res. ):.Cell-type specificity analysis of RNAP2-associated sites. (A) HepG2 CRE-seq activity for distinct classes of RNAP2-associated elements is shown as box plots. The log2-transformed CRE-seq activity (RNA/DNA barcode counts) is displayed on the y-axis. HepG2 CRE-seq activities are given for binding sites that are shared between HepG2 and K562 cells (Shared sites), as well as cell-type–specific sites that are found in only HepG2 cells (HepG2 only) or only in K562 cells (K562 only). Associated HepG2 CRE-seq activities of scrambled control sequences for each of the three classes of sites are also plotted. A key is given on the right of the graph. The percentage of elements from each of the three classes of sites above the 95th percentile of associated scrambled control sites are displayed on the plot. (B) K562 CRE-seq activity for distinct classes of RNAP2-associated elements is shown as box plots. The log2-transformed CRE-seq activity (RNA/DNA barcode counts) is displayed on the y-axis. K562 CRE-seq activities are given for binding sites that are shared between HepG2 and K562 cells (Shared sites), as well as cell-type–specific sites that are found in only HepG2 cells (HepG2 only) or only in K562 cells (K562 only). Associated K562 CRE-seq activities of scrambled control sequences for each of the three classes of sites are also plotted. A key is given on the right of the graph. The percentage of elements from each of the three classes of sites above the 95th percentile of associated scrambled control sites are displayed on the plot. (C) Spearman rank correlations between HepG2 and K562 CRE-seq activities for RNAP2-associated shared sites (Shared_Pol2), HepG2-specific sites (HepG2_Pol2), and K562-specific sites (K562_Pol2) are given. Shared sites exhibit positive correlation between CRE-seq activities in HepG2 and K562 cells, whereas cell-type–specific sites are not as strongly correlated (K562-specific sites) or negatively correlated (HepG2-specific sites).Genome Res. ):.Motif and functional genomic analyses of CEBPB binding sites. (A) Motif analysis depicts enrichment for the HNF4A motif at active (in red) and inactive (in purple) CEBPB-bound sites in HepG2 cells. Motif fold enrichments and P-values are given in the top right. The location and orientation from the center of each element is shown on the x-axis. (B) Motif analysis depicts enrichment for the FOSL2 motif at active (in red) and inactive (in purple) CEBPB-bound sites in HepG2 cells. (C) Motif analysis depicts enrichment for the ETS1 motif at active (in red) and inactive (in purple) CEBPB-bound sites in K562 cells.Genome Res. ):.Publication TypesSecondary Source IDGrant SupportFull Text Sources
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