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H3K4me3 ChIP_Seq in mouse decidua

ABSTRACT: H3K4me3 ChIP_Seq in mouse decidua

PROVIDER: PRJNA790987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17282696_1.fastq.gz	Fastqsanger.gz
	SRR17282696_2.fastq.gz	Fastqsanger.gz
	SRR17282697_1.fastq.gz	Fastqsanger.gz
	SRR17282697_2.fastq.gz	Fastqsanger.gz

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Project description:To detect the direct target genes of H3K4me3 in decidual stromal cells, decidual stromal cells are collected and subjected to ChIP-Seq. After aligned to mouse mm10 by STAR, peaks are called by MACS2. We found that H3K4me3 was significantly enriched at the transcription start site (TSS) of expressed genes (RPKM>1). A direct comparison of Menin and H3K4me3 ChIP-seq peaks at gene promoters showed a significantly strong positive correlation (R2=0.5888291). The promoters of 6,800 genes bound by Menin (92% of all genes with promoter bound by Menin) were also H3K4me3 modified.

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Project description:To detect the direct target genes of Menin and H3K4me3 in decidual stromal cells, decidual stromal cells are collected and subjected to ChIP-Seq. After aligned to mouse mm10 by STAR, peaks are called by MACS2. We found that Menin and H3K4me3 was significantly enriched at the transcription start site (TSS) of expressed genes (RPKM>1). A direct comparison of Menin and H3K4me3 ChIP-seq peaks at gene promoters showed a significantly strong positive correlation (R2=0.5888291). The promoters of 6,800 genes bound by Menin (92% of all genes with promoter bound by Menin) were also H3K4me3 modified.

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Project description:Our objective was to identify genes differentially expressed between control and Ezh2 cKO decidua, and to compare this set of genes with a previously identified gene set of H3K27me3-marked decidual genes that are putatively silenced by EZH2/PRC2 (Nancy et al. JCI. 2018). RNA was isolated from whole tissue decidua and myometrium of control and Ezh2 cKO mice. Sequencing provided was 731 million total reads with an average of 84.5% of these reads aligning uniquely to the mouse genome. Reads uniquely mapped to known mRNAs were used to identify gene expression changes between housing conditions using DESeq2. We found that 2530 protein-coding genes were differentially expressed within the decidua and 521 were differentially expressed in the myometrium (FDR<0.05, excluding genes whose normalized read counts were less than 30 averaged across samples). Hypergeometric analysis revealed a strong enrichment for previously identified H3K27me3 targets within genes overexpressed in Ezh2 cKO decidua.

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Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, by using mouse embryonic stem cells (mESCs) as a model system, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Notably, we show that H3K4me3 is required for the recruitment of the Integrator Complex Subunit 11 (INTS11), which is essential for the eviction of paused RNAPII and transcriptional elongation. Thus, our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.

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