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RNA polymerase mapping in plants identifies enhancers enriched in causal variants

ABSTRACT: RNA polymerase mapping in plants identifies enhancers enriched in causal variants

PROVIDER: PRJNA472570 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7195584.fastq.gz	Fastqsanger.gz
	SRR7195585.fastq.gz	Fastqsanger.gz

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RNA polymerase mapping in plants identifies enhancers enriched in causal variants

Project description:Promoter-proximal pausing and divergent transcription at promoters and enhancers, which are prominent features in animals, have been reported to be absent in plants based on a study of Arabidopsis thaliana. Here, our PRO-Seq analysis in cassava (Manihot esculenta) identified peaks of transcriptionally-engaged RNA polymerase II (Pol2) at both 5’ and 3’ ends of genes, consistent with paused or slowly-moving Pol2, and divergent transcription at potential intragenic enhancers. A full genome search for bi-directional transcription using an algorithm for enhancer detection developed in mammals (dREG) identified many enhancer candidates. These sites show distinct patterns of methylation and nucleotide variation based on genomic evolutionary rate profiling characteristic of active enhancers. Maize GRO-Seq data showed RNA polymerase occupancy at promoters and enhancers consistent with cassava but not Arabidopsis. Furthermore, putative enhancers in maize identified by dREG significantly overlapped with sites previously identified on the basis of open chromatin, histone marks, and methylation. As evidence of the functional relevance of these sites in cassava, we show that SNPs in them predict significantly more variation in fitness and root composition than SNPs in chromosomal segments randomly ascertained from the same intergenic distribution. The findings shed new light on plant transcription regulation and its impact on development and plasticity.

2018-06-21 | GSE114758 | GEO

Fine-mapping and functional studies highlight potential causal variants for rheumatoid arthritis and type 1 diabetes

Project description:We investigated whether variants fine-mapped for Rheumatoid Arthritis (RA) and Type 1 Diabetes overlap with open chromatin regions specifically after stimulation. We show that rs117701653, a potentially causal variant for RA near CD28, overlaps open chromatin regions only after stimulation. We futhermore observe a small increase in enhancer activity for this variant under stimulatory conditions using a luciferase assay. Reads were anonimized prior to upload.

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Redundant enhancers and causal variants in the TCF7L2 gene.

Project description: Not available

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Genome-wide enhancer-gene regulatory maps link causal variants to target genes underlying human colorectal cancer risk [RNA-seq]

Project description:Although GWASs have identified thousands of variants associated with human complex traits, most of which reside in the non-coding regions, especially enhancers, and biological mechanisms remain unclear. To created enhancer-gene maps to determine causal variant of CRC risk, we performed multi-omics analyses of ATAC-seq, H3K27ac ChIP-seq and RNA-seq with high quality from our 10 CRC tissues. By computationally integrating these multi-omics data, we identified 34,130 enhancer-gene connections involving 15,121 unique enhancers and 12,351 expressed genes. We demonstrated an ABC regulatory variant rs4810856 that is significantly associated with an increased CRC risk with large-scale population study and biological experiments. Our study provides regulation maps linking enhancers to genes, providing new insights into colorectal cancer etiology.

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Genome-wide enhancer-gene regulatory maps link causal variants to target genes underlying human colorectal cancer risk [ATAC-seq]

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Genome-wide enhancer-gene regulatory maps link causal variants to target genes underlying human colorectal cancer risk [H3K27ac ChIP-seq]

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Multiple causal variants underlie genetic associations in humans

Project description:Multiple causal variants underlie genetic associations in humans

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Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers.

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Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences

Project description:Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences

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Motif signatures in stretch enhancers are enriched for disease-associated genetic variants.

Project description:BACKGROUND:Stretch enhancers (SEs) are large chromatin-defined regulatory elements that are at least 3,000 base pairs (bps) long, in contrast to the median enhancer length of 800 bps. SEs tend to be cell-type specific, regulate cell-type specific gene expression, and are enriched in disease-associated genetic variants in disease-relevant cell types. Transcription factors (TFs) can bind to enhancers to modulate enhancer activity, and their sequence specificity can be represented by motifs. We hypothesize motifs can provide a biological context for how genetic variants contribute to disease. RESULTS:We integrated chromatin state, gene expression, and chromatin accessibility [measured as DNase I Hypersensitive Sites (DHSs)] maps across nine different cell types. Motif enrichment analyses of chromatin-defined enhancer sequences identify several known cell-type specific "master" factors. Furthermore, de novo motif discovery not only recovers many of these motifs, but also identifies novel non-canonical motifs, providing additional insight into TF binding preferences. Across the length of SEs, motifs are most enriched in DHSs, though relative enrichment is also observed outside of DHSs. Interestingly, we show that single nucleotide polymorphisms associated with diseases or quantitative traits significantly overlap motif occurrences located in SEs, but outside of DHSs. CONCLUSIONS:These results reinforce the role of SEs in influencing risk for diseases and suggest an expanded regulatory functional role for motifs that occur outside highly accessible chromatin. Furthermore, the motif signatures generated here expand our understanding of the binding preference of well-characterized TFs.

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