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H3K36me3 Modification by SETD2 is Essential for Col11a2 and Sema3e Transcription to Maintain Dentinogenesis in Mice

ABSTRACT: H3K36me3 Modification by SETD2 is Essential for Col11a2 and Sema3e Transcription to Maintain Dentinogenesis in Mice

PROVIDER: PRJNA1216905 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32162981_1.fastq.gz	Fastqsanger.gz
	SRR32162981_2.fastq.gz	Fastqsanger.gz
	SRR32162982_1.fastq.gz	Fastqsanger.gz
	SRR32162982_2.fastq.gz	Fastqsanger.gz
	SRR32162983_1.fastq.gz	Fastqsanger.gz

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H3K36me3 Modification by SETD2 is Essential for Col11a2 and Sema3e Transcription to Maintain Dentinogenesis in Mice

Project description:Dentin is a major mineralized component of teeth generated by odontoblasts. Several types of histone methylation have been reported to play important roles in odontoblast differentiation and dentinogenesis. However, the role of methylation on histone 3 at lysine 36 (H3K36) remains enigmatic. Here we find a high expression of SETD2, a methyltransferase catalyzing the trimethylation of H3K36 (H3K36me3), in the odontoblast layer. In vitro knockdown experiments and in vivo observations of two conditional knockout mouse models reveal SETD2 is essential for odontoblast differentiation and dentinogenesis. Integrated analyses of RNA sequencing and Spike-in Cleavage Under Targets and Tagmentation sequencing data show SETD2 is crucial for both H3K36me3 occupancy on the loci of Col11a2 and Sema3e and their transcription. Further experiments verify COL11A2 and SEMA3E act upstream of AKT1 signaling, promoting odontoblastic differentiation. In vitro and in vivo activation of AKT1 using SC79 (an AKT activator) partially rescues the impaired odontoblast differentiation caused by Setd2 knockdown or deficiency. Therefore, our findings indicate that H3K36me3 mediated by SETD2 is essential for dentinogenesis through regulating the expression of Col11a2 and Sema3e and AKT1 signaling.

2025-02-03 | GSE288311 | GEO

H3K36me3 Modification by SETD2 is Essential for Col11a2 and Sema3e Transcription to Maintain Dentinogenesis in Mice

2025-02-03 | GSE288310 | GEO

H3K36me3 Modification by SETD2 is Essential for Col11a2 and Sema3e Transcription to Maintain Dentinogenesis in Mice

Project description:H3K36me3 Modification by SETD2 is Essential for Col11a2 and Sema3e Transcription to Maintain Dentinogenesis in Mice

| PRJNA1216904 | 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

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

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

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

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

| PRJNA593576 | ENA

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

H3K36me3 and H3K27me3 occupancy profiling by high throughput sequencing from setd2 wt and ko germinal center B cells and H3K27me3 occupancy profiling by high throughput sequencing from phf19 wt and ko germinal center B cells

Project description:Our study aims to understand the H3K36me3 and H3K27me3 genome-wide alterations by analysing CHIP-seq data between setd2 wt and ko germinal center B cells, characterize the function of H3K36me3 methyltransferase setd2 in H3K36me3 itself and H3K27me3, further we aim to H3K27me3 from phf19 ,which is H3K27me3 regulator, WT and KO group to investigate the mechanism of H3K36me3 dependent H3K27me3 modification introduced by setd2.

2024-09-14 | GSE184043 | 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

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