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Altered Enhancer and Promoter Usage Leads to Differential Gene Expression in the Normal and Failed Human Heart

ABSTRACT: Altered Enhancer and Promoter Usage Leads to Differential Gene Expression in the Normal and Failed Human Heart

PROVIDER: PRJNA613478 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11351700.fastq.gz	Fastqsanger.gz
	SRR11351701.fastq.gz	Fastqsanger.gz
	SRR11351702.fastq.gz	Fastqsanger.gz
	SRR11351703.fastq.gz	Fastqsanger.gz
	SRR11351704_1.fastq.gz	Fastqsanger.gz

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Altered Enhancer and Promoter Usage Leads to Differential Gene Expression in the Normal and Failed Human Heart

Project description:The failed heart is characterized by re-expression of a fetal gene program, which contributes to adaptation and maladaptation in heart failure. To define genomewide enhancer and promoter use in heart failure, Cap Analysis of Gene Expression (CAGE-seq) was applied to healthy and failed human left ventricles to define short RNAs associated with both promoters and enhancers. Integration of CAGE-seq data with RNA sequencing identified a combined ~17,000 promoters and ~1,500 enhancers active in healthy and failed human left ventricles. Comparing promoter usage between healthy and failed hearts highlighted promoter shifts which altered amino-terminal protein sequences. Comparing enhancer usage between healthy and failed hearts revealed a majority of differentially utilized heart failure enhancers were intronic and primarily localized within the first intron, identifying this position as a common feature associated with tissue-specific gene expression changes in the heart. This dataset defines the dynamic genomic regulatory landscape underlying heart failure and serves as an important resource for understanding genetic contributions to cardiac dysfunction.

2020-09-01 | GSE147236 | GEO

Altered Enhancer and Promoter Usage Leads to Differential Gene Expression in the Normal and Failed Human Heart.

Project description:BackgroundThe failing heart is characterized by changes in gene expression. However, the regulatory regions of the genome that drive these gene expression changes have not been well defined in human hearts.MethodsTo define genome-wide enhancer and promoter use in heart failure, cap analysis of gene expression sequencing was applied to 3 healthy and 4 failed human hearts to identify promoter and enhancer regions used in left ventricles. Healthy hearts were derived from donors unused for transplantation and failed hearts were obtained as discarded tissue after transplantation.ResultsCap analysis of gene expression sequencing identified a combined potential for ≈23 000 promoters and ≈5000 enhancers active in human left ventricles. Of these, 17 000 promoters and 1800 enhancers had additional support for their regulatory function. Comparing promoter usage between healthy and failed hearts highlighted promoter shifts which altered aminoterminal protein sequences. Enhancer usage between healthy and failed hearts identified a majority of differentially used heart failure enhancers were intronic and primarily localized within the first intron, revealing this position as a common feature associated with tissue-specific gene expression changes in the heart.ConclusionsThis data set defines the dynamic genomic regulatory landscape underlying heart failure and serves as an important resource for understanding genetic contributions to cardiac dysfunction. Additionally, regulatory changes contributing to heart failure are attractive therapeutic targets for controlling ventricular remodeling and clinical progression.

| S-EPMC7577963 | biostudies-literature

Characterization of alternative promoter usage in advanced prostate cancer

Project description:In this study, we use deep whole genome transcriptome sequencing to show promoter activity changes during progression from normal prostate cells to advanced prostate disease. We show how androgen signaling and somatic alterations such as loss of the tumor suppressor RB1 or the activation of the ERG oncogene are linked to activity of transcription factors at noncanonical promoters. Alternative promoter usage analysis more accurately reflects changes in TF network during disease progression and in response to therapy. Lastly, we use matched whole genome methylation data to demonstrate a link between methylation and alternative promoter activity, dramatically improving the strength of association between gene expression and methylation data.

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Altered TE-derived genes leads to pathogenesis of FXD

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Altered enhancer-promoter interaction leads to MNX1 expression in pediatric acute myeloid leukemia with t(7 12)(q36 p13)

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SR0726 deletion leads to altered transcriptome of cultured Borrelia burgdorferi

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Altered enhancer-promoter interaction leads to MNX1 expression in pediatric acute myeloid leukemia with t(7 12)(q36 p13) [ATAC-Seq]

Project description:Altered enhancer-promoter interaction leads to MNX1 expression in pediatric acute myeloid leukemia with t(7 12)(q36 p13) [ATAC-Seq]

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