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Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

ABSTRACT: Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

PROVIDER: PRJNA705707 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13817107.fastq.gz	Fastqsanger.gz
	SRR13817108.fastq.gz	Fastqsanger.gz
	SRR13817109.fastq.gz	Fastqsanger.gz
	SRR13817110.fastq.gz	Fastqsanger.gz
	SRR13817111.fastq.gz	Fastqsanger.gz

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Similar Datasets

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

Project description:Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at active gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) GV oocytes using ultra-low input ChIP-seq, in complement to DNA methylation and gene expression analysis. Setd1b cKO oocytes showed a redistribution of H3K4me3, with a marked loss at active gene promoters associated with downregulated gene expression. Remarkably, many regions gained H3K4me3 in Setd1b cKOs, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich. All of these are hallmarks of MLL2 targets; thus, loss of SETD1B appears to enable enhanced MLL2 activity. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to transcriptional activity and MLL2 to CpG content.

2022-01-17 | GSE167986 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

2022-01-17 | GSE167985 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

2022-01-17 | GSE167984 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

Project description:Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

| PRJNA705713 | ENA

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

Project description:Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

| PRJNA705709 | ENA

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

Project description:Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

| PRJNA705711 | ENA

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-17 | GSE167987 | GEO

The histone 3 lysine 4 methyltransferase Setd1b is a maternal effect gene required for the oogenic gene expression program

Project description:Germ cell development involves major reprogramming of the epigenome to prime the zygote for totipotency. Histone 3 lysine 4 (H3K4) methylations are universal epigenetic marks mediated in mammals by six H3K4 methyltransferases related to fly Trithorax, including two yeast Set1 orthologs: Setd1a and Setd1b. Whereas Setd1a plays no role in oogenesis, we report that Setd1b deficiency causes female sterility. Oocyte specific Gdf9iCre conditional knockout (Setd1bGdf9cKO) ovaries develop through all stages however follicular loss accumulated with age and unfertilized metaphase II (MII) oocytes exhibited irregularities of the zona pellucida and meiotic spindle. Most Setd1bGdf9cKO zygotes remained in the pronuclear stage and displayed polyspermy in the perivitelline space. Expression profiling of Setd1bGdf9cKO MII oocytes revealed (i) that Setd1b promotes the expression of the major oocyte transcription factors including Obox1, 2, 5, 7, Meis2 and Sall4; and (ii) two-times more up- than downregulated mRNAs suggesting that Setd1b also promotes the expression of negative regulators of oocyte development with multiple Zfp-KRAB factors implicated. Together, these findings indicate that Setd1b serves as maternal effect gene through regulation of the oocyte gene expression program.

2017-02-09 | GSE85360 | GEO

Broad H3K4me3 controls transcription output and timing during spermatid development

Project description:Male germ cells express a complex transcriptome under tight temporal regulation during their development. However, our knowledge of the epigenetic regulation of crucial stages in this process, such as meiotic onset, remains limited. Here, by dissecting a comprehensive map of the dynamic epigenomic landscape in developing mouse male germ cells, we uncover mutually exclusive shifts in the repressive histone marks H3K9me2, H3K9me3 and H3K27me3 during the mitosis-to-meiosis transition and completion of meiotic recombination. These dynamic shifts coincide with temporal changes in global transcriptional output, retrotransposon activity, and the silencing of mitotic/meiotic genes during spermatogenesis. In addition, we identify Setd1b-mediated broad H3K4me3 domains in both mouse and human spermatids. These broad H3K4me3 domains promote Pol II occupancy and transcription, resulting in high gene expression in spermatids. Setd1b ablation leads to a complete loss of broad H3K4me3, and the redistribution of Pol II from broad H3K4me3 promoters to regular H3K4me3 promoters, thereby compromising temporal gene expression and ultimately hampering spermiogenesis. These findings reveal that dynamic epigenetic changes orchestrate stage-specific gene expression in spermatogenesis, with Setd1b-mediated broad H3K4me3 serving as a crucial regulator that controls the timing of stage-specific gene expression in spermatids.

2024-09-03 | GSE242515 | GEO

Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes [WT scRNA-seq]

Project description:Histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Amongst these enzymes SET domain containing 1b (SETD1B) has been linked to syndromic intellectual disability but its role in the postnatal brain has not been studied yet. Here we employ mice that lack Setd1b from excitatory neurons of the postnatal forebrain and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that SETD1B controls the expression of genes with a broad H3K4me3 peak at their promoters that represent neuronal enriched genes linked to learning and memory function. Comparative analysis to corresponding data from conditional Kmt2a and Kmt2b knockout mice suggests that this function is specific to SETD1B. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-mediated regulation of H3K4me levels in postnatal neurons is critical for cognitive function.

2021-12-17 | GSE185182 | GEO

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