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NR2F2 genome occupancy and the H3K4me1 histone mark profile in the mouse uterus at gestation day 3.5

ABSTRACT: NR2F2 genome occupancy and the H3K4me1 histone mark profile in the mouse uterus at gestation day 3.5

PROVIDER: PRJNA972760 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24572187.fastq.gz	Fastqsanger.gz
	SRR24572188.fastq.gz	Fastqsanger.gz
	SRR24572189.fastq.gz	Fastqsanger.gz
	SRR24572190.fastq.gz	Fastqsanger.gz

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NR2F2 genome occupancy and the H3K4me1 histone mark profile in the mouse uterus at gestation day 3.5

Project description:NR2F2 genome occupancy and H3K4me1 histone mark profiles in the prereceptive stage of the pregnant mouse uterine specimens were documented by ChIP-seq to investigate downstream targets of the NR2F2 and candidate partner transcription regulators.

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Nr2f2 deficiency in Pgr-expressing cells NR2F2 genome occupancy and the H3K4me1 histone mark uterus at gestation day 3.5

Project description:Nr2f2 deficiency in Pgr-expressing cells NR2F2 genome occupancy and the H3K4me1 histone mark uterus at gestation day 3.5

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Nr2f2 deficiency in Pgr-expressing cells; NR2F2 genome occupancy and the H3K4me1 histone mark; uterus at gestation day 3.5

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Uterine transcriptomic profiles of Nr2f2 deficiency in Pgr-expressing cells at gestation day 3.5

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Uterine transcriptomic profiles of Nr2f2 deficiency in Pgr-expressing cells at gestation day 3.5

Project description:Endometrial epithelia and stroma communicate via progesterone and estrogen signaling to prepare a receptive uterus for embryo implantation in early pregnancy. The present study determines, in early pregnancy at the prereceptive stage, the uterine gene signature of the NR2F2 transcription factor that is crucial for mediating the progesterone dependent anti-proliferative actions in the epithelia.

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Differential chromatine state and ER binding potentially induced by NR2F2 depletion.

Project description:ERα binding activity largely depends on access to binding sites on chromatin, which is facilitated in part by Pioneer Factors (PFs).We show that most binding events of NR2F2 occur together with the ERα binding sites.To explore whether NR2F2 may act as potential pioneer factor of ER, we performed a series of ChIP-seq genome wide in MCF-7. Since NR2F2 associates with chromatin prior to estrogen treatment and its depletion in MCF-7 cells did not affect ERα expression, we hypothesize NR2F2 may inhibit estrogen-dependent growth by modulating ERα recruitment. We performed ChIP-seq genome wide gainst ERα before and after NR2F2 depletion.Covalent modifications are a main chromatin property.To test whether NR2F2 favoured histone modification deposition on chromatin, we profiled ChIP-Seq of H3K4me1, H3K4me3, and H3K27ac following NR2F2 depletion in oestrogen-starved MCF-7 cells to gain comprehensive histone medication landscape.

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ZMYND8 reads the dual histone mark H3K4me1-H3K14ac to antagonize the expression of metastasis-linked genes

Project description:Histone acetylation, including acetylated H3K14 (H3K14ac), is generally linked to gene activation. Monomethylated histone H3 lysine 4 (H3K4me1), together with other gene-activating marks, denotes active genes. In contrast to usual gene-activating functions of H3K14ac and H3K4me1, we here show that the dual histone modification mark H3K4me1-H3K14ac is recognized by ZMYND8 (also called RACK7) and functions to counteract gene expression. We identified ZMYND8 as a transcriptional corepressor of the H3K4 demethylase JARID1D. ZMYND8 antagonizes the expression of metastasis-linked genes, and its knockdown increases the cellular invasiveness in vitro and in vivo. The plant homeodomain (PHD) and Bromodomain cassette in ZMYND8 mediates the combinatorial recognition of H3K4me1-H3K14ac and H3K4me0-H3K14ac by ZMYND8. These findings uncover an unexpected role for the signature H3K4me1-H3K14ac in attenuating gene expression and reveal a previously unknown metastasis-suppressive epigenetic mechanism in which ZMYND8's PHD-Bromo cassette couples H3K4me1-H3K14ac with repression of metastasis-linked genes. i) ChIP-Seq data of ZMYND8, JARID1D, H3K4me1, H3K14ac, H3K4me3, and H3K27me3 in normal DU145 cells. ii) ChIP-Seq data of H3K4me1 and H3K4me3 in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells. iii) RNA-Seq data in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells.

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H3K27ac and H3K4me1 histone mark profiles in term pregnant human myometrial tissues

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ZMYND8 reads the dual histone mark H3K4me1-H3K14ac to antagonize the expression of metastasis-linked genes

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