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H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

ABSTRACT: H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

PROVIDER: PRJNA544440 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9029871_1.fastq.gz	Fastqsanger.gz
	SRR9029871_2.fastq.gz	Fastqsanger.gz
	SRR9029872_1.fastq.gz	Fastqsanger.gz
	SRR9029872_2.fastq.gz	Fastqsanger.gz
	SRR9029873_1.fastq.gz	Fastqsanger.gz

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H3K36 methyltransferase SETD2 regulates lymphoid and neural development [seq]

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H3K36 methyltransferase SETD2 regulates lymphoid and neural development [MIXCR]

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H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

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

2020-03-23 | GSE131690 | GEO

H3K36 methyltransferase SETD2 regulates lymphoid and neural development [seq]

Project description:We study the role of loss of Setd2 and H3K36me3 in early B cell development through NGS methods including RNA, ChIP and ATAC Seq of sorted B cell populations of control and Setd2KO primary B cells from mice.

2020-03-23 | GSE130904 | GEO

Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]

Project description:SETD2/HYPB has been known as a histone H3K36 specific methyltransferase. However, its roles in physiology such as development and cellular function remain unclear. In this study, using mESCs as cellular model, we show that Setd2 mainly regulates differentiation of murine embryonic stem cells (mESCs) towards primitive endoderm. This study aimed at exploring how did Setd2 regulate primitive endoderm. differentiation. We used microarrays to detail the global programme of gene expression controled by setd2, which is required for endoderm differentiation. Wild type and Setd2 knockout mESCs were selected for RNA extraction and hybridization on Affymetrix GeneChip® mouse genome 430 2.0 arrays. We sought to obtain some deregulated genes, which were required for primitive endoderm differentiation. For comparison, three biological repeats of each were performed.

2014-10-14 | E-GEOD-54931 | biostudies-arrayexpress

Loss of H3K36 Methyltransferase SETD2 Impairs V(D)J Recombination during Lymphoid Development.

Project description:Repair of DNA double-stranded breaks (DSBs) during lymphocyte development is essential for V(D)J recombination and forms the basis of immunoglobulin variable region diversity. Understanding of this process in lymphogenesis has historically been centered on the study of RAG1/2 recombinases and a set of classical non-homologous end-joining factors. Much less has been reported regarding the role of chromatin modifications on this process. Here, we show a role for the non-redundant histone H3 lysine methyltransferase, Setd2, and its modification of lysine-36 trimethylation (H3K36me3), in the processing and joining of DNA ends during V(D)J recombination. Loss leads to mis-repair of Rag-induced DNA DSBs, especially when combined with loss of Atm kinase activity. Furthermore, loss reduces immune repertoire and a severe block in lymphogenesis as well as causes post-mitotic neuronal apoptosis. Together, these studies are suggestive of an important role of Setd2/H3K36me3 in these two mammalian developmental processes that are influenced by double-stranded break repair.

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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

Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]

2014-10-14 | GSE54931 | GEO

Systematic perturbations of SETD2, NSD1, NSD2, NSD3 and ASH1L reveals their distinct contributions to H3K36 methylation

Project description:Methylation of histone 3 lysine 36 (H3K36me) has emerged as an essential epigenetic component for the faithful regulation of gene expression. Despite its demonstrated importance in development, disease, and cancer, the molecular agents responsible for the deposition of H3K36me are not yet well understood. Here, we use a mouse mesenchymal stem cell model to comprehensively perturb the components of the H3K36me deposition machinery and infer the activities of the five most prominent players: SETD2, NSD1, NSD2, NSD3, and ASH1L. We find that H3K36me2 is the most abundant of the three methylation states and that it is predominantly deposited at intergenic regions by NSD1, and in part by NSD2. In contrast, H3K36me1/3 are most abundant within exons and have a positive correlation with gene expression. We further demonstrate that while SETD2 is responsible for depositing most H3K36me3, it also deposits a modest amount of H3K36me2 within transcribed genes. Additionally, loss of SETD2 results in an increase of exonic H3K36me1, suggesting that other H3K36 methyltransferases may prime gene bodies with lower methylation states ahead of transcription. Through a reductive approach, we uncover the genome-wide distribution patterns of NSD3- and ASH1L-catalyzed H3K36me2. While NSD1/2 establish broad intergenic H3K36me2 domains, NSD3 deposits broad H3K36me2 peaks centered on active promoter and enhancer regions. Meanwhile, the activity of ASH1L is focused primarily on the promoters of developmentally relevant genes, and our analyses implicate PBX2 as a potential recruitment factor for ASH1L to these regions. Overall, our study provides new insights into the regulation of H3K36me by the H3K36 methyltransferase family and helps to consolidate the wealth of previous observations in the context of a structured analysis.

2023-10-05 | MSV000093049 | MassIVE

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