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H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE131690 | GEO | 2020/03/23

REPOSITORIES: GEO

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H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

Project description:H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

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H3K36 methyltransferase SETD2 regulates lymphoid and neural development [MIXCR]

Project description:Complete Amplicon Sequencing of a 500bp V(D)J recombination products from proB cells sorted from control and Setd2KO mice to Vh558, Vh7183 and Vhq52 variable gene familes to JH4 joining gene fragment to determine CDR3

2020-03-23 | GSE131608 | 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

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.

| S-EPMC7066224 | biostudies-literature

H3K36 methyltransferase SETD2 regulates lymphoid and neural development [RNA-seq]

Project description:Transcript analysis of RNA from murine proB cells to determine B cell repertoire and variable gene usage

2020-03-23 | GSE131588 | GEO

H3K36 methyltransferase SETD2 regulates lymphoid and neural development [MIXCR]

Project description:H3K36 methyltransferase SETD2 regulates lymphoid and neural development [MIXCR]

| PRJNA544179 | ENA

H3K36 methyltransferase SETD2 regulates lymphoid and neural development [seq]

Project description:H3K36 methyltransferase SETD2 regulates lymphoid and neural development [seq]

| PRJNA541930 | ENA

H3K36 methyltransferase SETD2 regulates lymphoid and neural development [RNA-seq]

Project description:H3K36 methyltransferase SETD2 regulates lymphoid and neural development [RNA-seq]

| PRJNA544097 | ENA

Histone Lysine Methyltransferase SETD2 Regulates Coronary Vascular Development in Embryonic Mouse Hearts.

Project description:Congenital heart defects are the most common birth defect and have a clear genetic component, yet genomic structural variations or gene mutations account for only a third of the cases. Epigenomic dynamics during human heart organogenesis thus may play a critical role in regulating heart development. However, it is unclear how histone mark H3K36me3 acts on heart development. Here we report that histone-lysine N-methyltransferase SETD2, an H3K36me3 methyltransferase, is a crucial regulator of the mouse heart epigenome. Setd2 is highly expressed in embryonic stages and accounts for a predominate role of H3K36me3 in the heart. Loss of Setd2 in cardiac progenitors results in obvious coronary vascular defects and ventricular non-compaction, leading to fetus lethality in mid-gestation, without affecting peripheral blood vessel, yolk sac, and placenta formation. Furthermore, deletion of Setd2 dramatically decreased H3K36me3 level and impacted the transcriptional landscape of key cardiac-related genes, including Rspo3 and Flrt2. Taken together, our results strongly suggest that SETD2 plays a primary role in H3K36me3 and is critical for coronary vascular formation and heart development in mice.

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H3K36 methyltransferase NSD1 regulates chondrocyte differentiation for skeletal development and fracture repair.

Project description:Chondrocyte differentiation is a critical process for endochondral ossification, which is responsible for long bone development and fracture repair. Considerable progress has been made in understanding the transcriptional control of chondrocyte differentiation; however, epigenetic regulation of chondrocyte differentiation remains to be further studied. NSD1 is a H3K36 (histone H3 at lysine 36) methyltransferase. Here, we showed that mice with Nsd1 deficiency in Prx1+ mesenchymal progenitors but not in Col2+ chondrocytes showed impaired skeletal growth and fracture healing accompanied by decreased chondrogenic differentiation. Via combined RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) analysis, we identified sex determining region Y box 9 (Sox9), the key transcription factor of chondrogenic differentiation, as a functional target gene of NSD1. Mechanistically, NSD1 regulates Sox9 expression by modulating H3K36me1 and H3K36me2 levels in the Sox9 promoter region, constituting a novel epigenetic regulatory mechanism of chondrogenesis. Moreover, we found that NSD1 can directly activate the expression of hypoxia-inducible factor 1α (HIF1α), which plays a vital role in chondrogenic differentiation through its regulation of Sox9 expression. Collectively, the results of our study reveal crucial roles of NSD1 in regulating chondrogenic differentiation, skeletal growth, and fracture repair and expand our understanding of the function of epigenetic regulation in chondrogenesis and skeletal biology.

| S-EPMC8185073 | biostudies-literature

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