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

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

PROVIDER: PRJNA433473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6686550.fastq.gz	Fastqsanger.gz
	SRR6686551.fastq.gz	Fastqsanger.gz
	SRR6686552.fastq.gz	Fastqsanger.gz
	SRR6686553.fastq.gz	Fastqsanger.gz
	SRR6686546.fastq.gz	Fastqsanger.gz

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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

Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

Project description:Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

| PRJNA433476 | ENA

setd2 knockout zebrafish is survivable and fertile: differential and developmental-stress-related requirements for Setd2 and histone H3K36 trimethylation in different vertebrate animals

Project description:Setd2 is the only enzyme that catalyzes histone H3 lysine 36 trimethylation (H3K36me3) on virtually all actively transcribed protein-coding genes, and this mechanism is evolutionarily conserved from yeast to human. Setd2 and H3K36me3 have been revealed to be involved in many important biochemical mechanisms, including DNA repair, alternative mRNA splicing and transcription elongation. However, physiological function of Setd2 in the context of zebrafish development remains elusive. Here we generated zebrafish setd2 mutant lines through disrupting the majority of the protein. And mRNA profiles of wild-type (WT), Setd2(+/-) and Setd2(-/-) zebrafish embryos at 36hpf were generated by deep sequencing, providing an opportunity to uncover molecular programs and functions of Setd2.

2020-05-27 | GSE151238 | GEO

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

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

| PRJNA433475 | ENA

Splicing enhances recruitment of methyltransferase HYPB/Setd2 and methylation of histone H3 lysine 36

Project description:Several lines of recent evidence support a role for chromatin in splicing regulation. Here we show that splicing can also contribute to histone modification, which implies a bidirectional communication between epigenetics and RNA processing. Genome-wide analysis of histone methylation in human cell lines and mouse primary T cells reveals that intron-containing genes are preferentially marked with H3K36me3 relative to intronless genes. In intron-containing genes, H3K36me3 marking is proportional to transcriptional activity, whereas in intronless genes H3K36me3 is always detected at much lower levels. Furthermore, splicing inhibition impairs recruitment of H3K36 methyltransferase HYPB/Setd2 and reduces H3K36me3, whereas splicing activation has the opposite effect. Moreover, the increase of H3K36me3 correlates with the length of the first intron, consistent with the view that splicing enhances H3 methylation. We propose that splicing is mechanistically coupled to recruitment of HYPB/Setd2 to elongating RNA Polymerase II. This experiment proposes to profile genome-wide binding profiles by ChIP-seq (Illumina, 36 bp tags) of RNA polymerase II (one biological replicate), the histone modification H3K36me3 (2 replicates) and a reference control input sample (genomic DNA after reverse cross-link, one replicate) in a human H1299 lung carcinoma cell line *** Raw data not provided for Samples GSM766322-GSM766324.

2011-07-25 | E-GEOD-30902 | biostudies-arrayexpress

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 occupancy profiling by high throughput sequencing from control(APCmin) and APCmin; Setd2IEC-/- mice intestinal cells [ChIP-seq]

Project description:Setd2 catalyzes trimethylation of lysine 36 on histone H3. We conduct ChIP sequencing in chromatin landscape induced by Setd2 depleted in mouse intestinal cells to understand the H3K36me3 genome-wide alterations.

2017-09-01 | GSE95662 | GEO

SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters

Project description:Histone mark, one carrier of epigenetic information, regulates the gene expression in cells. Studies have shown that H3K36me3 is mainly catalyzed by SETD2 to be deposited at gene body regions in mammalian cells. Here, we profile the distributions of H3K36me3 in native cells and uncover that H3K36me3 is also enriched at the promoters beyond the gene body regions. We identify SMYD5 as one methyltransferase responsible for the enrichment of H3K36me3 at promoters. Through RNA polymerase II, SMYD5 is recruited to chromatin to regulate H3K36me3 and gene expression. The enzymatic activity of SMYD5 is dependent on its C-terminal glutamic acid rich domain. Depletion of C-terminal domain reduces the reestablishment of H3K36me3 at promoters when Smyd5 is over-expressed in Smyd5 knockout cells. Furthermore, elevated Smyd5 expression contributes to the tumorigenesis of liver hepatocellular carcinoma. Together, our study reveals SMYD5 as the H3K36me3 methyltransferase at promoters to regulate the gene expression, providing important insights into the localization and function of H3K36me3.

2022-04-26 | GSE184894 | GEO

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