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Mapping cis-regulatory elements in the midgestation mouse placenta

ABSTRACT: Mapping cis-regulatory elements in the midgestation mouse placenta

PROVIDER: PRJNA744555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15065800.fastq.gz	Fastqsanger.gz
	SRR15065801.fastq.gz	Fastqsanger.gz
	SRR15065802.fastq.gz	Fastqsanger.gz
	SRR15065803.fastq.gz	Fastqsanger.gz
	SRR15065804.fastq.gz	Fastqsanger.gz

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Mapping cis-regulatory elements in the midgestation mouse placenta.

Project description:The placenta is a temporary organ that provides the developing fetus with nutrients, oxygen, and protection in utero. Defects in its development, which may be caused by misregulated gene expression, can lead to devastating outcomes for the mother and fetus. In mouse, placental defects during midgestation commonly lead to embryonic lethality. However, the regulatory mechanisms controlling expression of genes during this period have not been thoroughly investigated. Therefore, we generated and analyzed ChIP-seq data for multiple histone modifications known to mark cis-regulatory regions. We annotated active and poised promoters and enhancers, as well as regions generally associated with repressed gene expression. We found that poised promoters were associated with neuronal development genes, while active promoters were largely associated with housekeeping genes. Active and poised enhancers were associated with placental development genes, though only active enhancers were associated with genes that have placenta-specific expression. Motif analysis within active enhancers identified a large network of transcription factors, including those that have not been previously studied in the placenta and are candidates for future studies. The data generated and genomic regions annotated provide researchers with a foundation for future studies, aimed at understanding how specific genes in the midgestation mouse placenta are regulated.

| S-EPMC8595355 | biostudies-literature

Epigenetic Mapping of Cis-Regulatory Elements in the Developing Mouse and Pig Forelimbs.

Project description:Epigenetic Mapping of Cis-Regulatory Elements in the Developing Mouse and Pig Forelimbs.

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Mapping cis-regulatory elements in the midgestation mouse placenta

Project description:We generated and analyzed ChIP-seq data for H3k4me3, H3k4me1, and H3k27me3. We annotated active and poised promoters and enhancers, as well as regions associated with repressed gene expression and found that poised promoters were associated with neuronal development genes, while active promoters were largely associated with housekeeping genes. Active and poised enhancers were associated with placental development genes, though only active enhancers were associated with genes that have placenta-specific expression.

2021-11-30 | GSE179695 | GEO

Effects of cis-regulatory elements on proteome

Project description:Background Genomic variations contribute to the phenotypic diversity of individuals. A number of polymorphisms in protein-coding regions that alter drug efficacy or lead to adverse reactions have been characterized; however, noncoding regions that affect drug responses are largely overlooked, except for a limited number of well-studied enhancers. Results We conducted a quantitative assessment of cis-regulatory elements (CREs) based on transcription initiation profiling of mRNAs and noncoding RNAs, including enhancer RNAs, by using CAGE (Cap Analysis of Gene Expression). Candidate CREs identified in a hepatocellular carcinoma HepG2 cell line with stable expression of drug-responsive transcription factor pregnane X receptor (PXR) were further narrowed down by integrating data of PXR-binding sites in human primary hepatocytes and genome-wide association studies. We found more than 100-fold enrichments of the candidates to genetically associated loci with circulating levels of bilirubin and vitamin D, which implicated a link to adverse reactions of PXR ligands. We uncovered novel enhancers of UGT1A1 and TSKU through CRISPR/Cas9 knockout experiments. We identified alleles altering regulatory activities of UGT1A1 and CYP24A1enhancers by using luciferase reporter assay. Furthermore, our siRNA experiments revealed an unexpected impact of TSKU on the expression of vitamin D-metabolizing enzymes. Conclusions Our transcriptome-based assessment of CREs expanded the list of drug-inducible and PXR-mediated enhancers and super-enhancers. We identified regulatory alleles that alter drug-induced gene expressions, and discovered a novel molecular cascade associated with an adverse reaction. Our results contribute a precise understanding of the noncoding elements of the human genome underlying drug responses.

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