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H3K4me3 ChIP_Seq in mouse decidua

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE191327 | GEO | 2022/01/20

REPOSITORIES: GEO

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Menin and H3K4me3 ChIP_Seq in mouse decidua

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:Menin and H3K4me3 ChIP_Seq in mouse decidua

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H3K4me3 ChIP_Seq in mouse decidua

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Histone H3K4me3 signal breadth reveals constitutive and hypoxia stress responsive endometrial functions linked to endometriosis

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Project description:Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. To study the role of menin-dependent H3K4me3, we performed in vitro differentiation of wild-type as well as menin-null mouse embryonic stem cells (mESCs) into pancreatic islet-like endocrine cells (PILECs). Gene expression analysis and genome-wide H3K4me3 ChIP-Seq profiling in wild-type and menin-null mESCs and PILECs revealed menin-dependent H3K4me3 at the imprinted Dlk1-Meg3 locus in mESCs, and all four Hox loci in differentiated PILECs. Specific and significant loss of H3K4me3 and gene expression was observed for genes within the imprinted Dlk1-Meg3 locus in menin-null mESCs and the Hox loci in menin-null PILECs. Given that the reduced expression of genes within the DLK1-MEG3 locus and the HOX loci is associated with MEN1-like sporadic tumors, our data suggests a possible role for menin-dependent H3K4me3 at these genes in the initiation and progression of sporadic pancreatic endocrine tumors. Furthermore, our investigation also demonstrates that menin-null mESCs can be differentiated in vitro into islet-like endocrine cells, underscoring the utility of menin-null mESC-derived specialized cell types for genome-wide high-throughput studies. Genome-wide mapping of H3K4me3 and microarray gene expression profiling in TC-1 wild-type (WT) mESCs, menin-null (Men1-ko) mESCs (3.2N), pancreatic islet-like endocrine cells (PILECs) derived from WT mESCs, and PILECs derived from Men1-ko mESCs.

2012-06-01 | E-GEOD-37774 | biostudies-arrayexpress

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA)

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