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Setd2-dependent H3K36me3 is required for Acrbp1 and protamine transcriptions and spermiogenesis in mice

ABSTRACT: Setd2-dependent H3K36me3 is required for Acrbp1 and protamine transcriptions and spermiogenesis in mice

PROVIDER: PRJNA428362 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6437440_1.fastq.gz	Fastqsanger.gz
	SRR6437440_2.fastq.gz	Fastqsanger.gz
	SRR6437441_1.fastq.gz	Fastqsanger.gz
	SRR6437441_2.fastq.gz	Fastqsanger.gz
	SRR6437442_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Setd2-dependent H3K36me3 is required for Acrbp1 and protamine transcriptions and spermiogenesis in mice

Project description:Spermatogenesis is precisely cotrolled by complex gene expression programs and involves epigenetic reprogramming including histone modification and DNA methylation. Setd2 catalyzes the trimethylation of histone H3 Lys36 (H3K36me3) and plays key roles in embryonic stem cell differentiation and somatic cell development; however, its role in male germ cell development remains elusive. Here we demonstrate an essential role of Setd2 for spermiogenesis. We show that targeted knockout of Setd2 in germ cells causes aberrant spermiogenesis with acrosomal malformation before step 8 round spermatid stage, resulting in complete male infertile. Furthermore, we show a complete loss of H3K36me3 and a significant altered gene expression profile, including Acrbp1 and protamines, caused by Setd2 deficiency. Our findings reveal a previously underappreciated role of Setd2-dependent H3K36me3 for spermiogenesis and improved the understanding of epigenetic disorders underlying male infertility.

2018-04-28 | GSE108717 | GEO

PHF7 Modulates BRDT Stability and Histone-to-Protamine Exchange during Spermiogenesis

Project description:Spermatogenesis is a complex process of sperm generation, including mitosis, meiosis, and spermiogenesis. During spermiogenesis, histones in post-meiotic spermatids are removed from chromatin and replaced by protamines. Although histone-to-protamine exchange is important for sperm nuclear condensation, the underlying regulatory mechanism is still poorly understood. Here, we identify PHD finger protein 7 (PHF7) as an E3 ubiquitin ligase for histone H3K14 in post-meiotic spermatids. Generation of Phf7-deficient mice and Phf7 C160A knockin mice with impaired E3 ubiquitin ligase activity reveals defects in histone-to-protamine exchange caused by dysregulation of histone removal factor Bromodomain, testis-specific (BRDT) in early condensing spermatids. Surprisingly, E3 ubiquitin ligase activity of PHF7 on histone ubiquitination leads to stabilization of BRDT by attenuating ubiquitination of BRDT. Collectively, our findings identify PHF7 as a critical factor for sperm chromatin condensation and contribute to mechanistic understanding of fundamental phenomenon of histone-to-protamine exchange and potential for drug development for the male reproduction system.

2020-07-28 | GSE136752 | GEO

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3. To obtain SETD2-dependent landscape of H3K36me3 in human genome, we performed ChIP sequencing in SETD2 silenced and control HepG2 cells.

2019-02-21 | GSE110318 | GEO

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Setd2 is the specific methyltransferase of H3K36me3. To obtain Setd2-dependent landscape of H3K36me3 in mouse genome, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed ChIP sequencing in mESCs with or without Dox treatment.

2019-02-21 | GSE110321 | GEO

Global transcriptome profiling of SETD2 and hnRNP L depleted cells and H3K36me3 profile of WT 293T cells

Project description:We performed RNA-seq of 293T cells post depletion and SETD2 or hnRNP L to compare their global transcriptome profile. We also looked at the distribution of the histone mark H3K36me3 in wild type 293T to correlate it with the observed transcriptome changes upon SETD2 and hnRNP L depletion. We rescued SETD2 knock out 293T cells with SETD2 FL (Full Length), FLΔSRI (FLwoSRI) and FLΔSHI (FLwoSHI) and performed H3K36me3 ChIP-Seq.

2021-01-29 | GSE151296 | GEO

PHF7 Modulates BRDT Stability and Histone-to-Protamine Exchange during Spermiogenesis

Project description:PHF7 Modulates BRDT Stability and Histone-to-Protamine Exchange during Spermiogenesis

| PRJNA563578 | ENA

Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

Project description:Purpose: The goal of this study is to identify differential Setd2-mediated H3K36me3 modificaion in the resolution phase of inflammation induced by LPS Methods: We profiled chip-seq with H3K36me3 antibody in bone marrow-derived macrophages stimulated with LPS for 0h, 4h, 16h. Results: We find different H3K36me3 enrichment peaks under LPS stimulation at different time.

2024-11-13 | GSE141470 | GEO

The SPOP-containing Complex Functions as an E3 Ligase for SETD2 to Regulate Gene-Specific H3K36me3-Coupled Alternative Splicing

Project description:H3K36me3 has been reported to associate with active gene expression, and SETD2 is the mainly methyltransferase for H3K36me3. We identified SPOP which is a CUL3 family protein as a E3 ligase for SETD2. Genome wide analysis by using ChIPSeq and RNASeq demonstrate that SPOP specificly eliminate H3K36me3 modification at target genes and resulted in alternative splicing of those target genes.

2016-11-10 | GSE75270 | GEO

H3K36me3 ChIP profiles of Setd2 fl/fl BMSCs infected with lentivirus expressing GFP and Cre

Project description:During the aging process, bone marrow mesenchymal stem cells (BMSCs) exhibit declined osteogenesis accompanied by excess adipogenesis, which will lead to osteoporosis. Here we report that the H3K36 trimethylation, catalyzed by histone methyltransferase SETD2 regulates lineage commitment of BMSCs. Deletion of Setd2 in mBMSCs, through conditional Cre expression driven by Prx1 promoter, resulted in bone loss and marrow adiposity. Loss of Setd2 in BMSCs in vitro facilitated differentiation propensity to adipocytes rather than to osteoblasts. Through conjoint analysis of RNA-seq and ChIP-seq data, we identified a SETD2 functional target gene, Lbp, on which H3K36me3 was enriched, and its expression was affected by Setd2 deficiency. Furthermore, overexpression of LBP could partially rescue the lack of osteogenesis and enhanced adipogenesis resulted from the absence of Setd2 in BMSCs. Further mechanism study demonstrated that the trimethylation level of H3K36 could regulate Lbp transcriptional initiation and elongation. These findings suggest that H3K36 trimethylation mediated by SETD2 could regulate the cell fate of mesenchymal stem cells in vitro and in vivo, indicating that the regulation of H3K36me3 level by targeting SETD2 and/or the administration of downstream LBP protein may represent potential therapeutic way for new treatment in metabolic bone diseases, such as osteoporosis.

2018-11-08 | GSE120351 | GEO

CUT&Tag analysis of H3K36me3 and H3K27me3, in Setd2-WT and -KO murine PDAC cell line

Project description:To gain mechanistic insight into how Setd2 loss promotes activation of AKT signaling, we performed CUT&Tag sequencing in PDAC cells (KPC1199) with Setd2-KO and Setd2-WT). Setd2-WT and -KO murine PDAC cells were cultured and freshly collected as soon as possible. Hyperactive pA-Tn5 Transposase for CUT&Tag kit from Vazyme (TD901), and antibodies against H3K36me3 and H3K27me3 were employed. Trueprep index kit v2 and v3 for illumina were used to establish DNA library.

2023-02-06 | GSE176013 | GEO

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