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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE131588 | GEO | 2020/03/23

REPOSITORIES: GEO

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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.

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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

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 [seq]

Project description: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 lymphoid and neural development [RNA-seq]

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

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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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Dynamic changes of SETD2, a histone H3K36 methyltransferase, in porcine oocytes, IVF and SCNT embryos.

Project description:SETD2 (SET domain containing protein 2) acts as a histone H3 lysine 36 (H3K36)-specific methyltransferase and may play important roles in active gene transcription in human cells. However, its expression and role in porcine oocytes and preimplantation embryos are not well understood. Here, we used immunofluorescence and laser scanning confocal microscopy to examine SETD2 expression in porcine fetal fibroblasts, oocytes, and preimplantation embryos derived from in vitro fertilization (IVF), parthenogenetic activation (PA), and somatic cell nuclear transfer (SCNT). In porcine fetal fibroblasts, SETD2 expression was detected in interphase cells, but not in M (mitotic)-phase cells. The SETD2 signal was observed in non-surrounded nucleolus (NSN)-stage oocytes, but not in surrounded nucleolus (SN)-, metaphase I (MI)-, or metaphase II (MII)-stage oocytes. The SETD2 signal was detectable in sperm, and undetectable immediately after fertilization, detectable at the 2-cell stage, and peaked at the 4-cell stage of IVF embryos in which porcine embryonic genome is activated. Similar to the pattern found in IVF embryos, the SETD2 signal was absent from PA embryos at the 1-cell stage, but it was detected at the 2-cell stage and thereafter maintained to the blastocyst stage. Interestingly, unlike the IVF and PA embryos, the SETD2 signal was detected throughout the development of SCNT embryos, including at the 1-cell stage. These data suggest that SETD2 may be functional for embryonic gene transcription in porcine preimplantation embryos. It is further speculated that the aberrant expression of SETD2 at the 1-cell stage of porcine SCNT embryos may be a factor in the low efficiency of cloning in pig.

| S-EPMC5813925 | biostudies-literature

The histone methyltransferase SETD2 negatively regulates cell size.

Project description:Cell size varies between cell types but is tightly regulated by cell intrinsic and extrinsic mechanisms. Cell size control is important for cell function, and changes in cell size are frequently observed in cancer. Here, we uncover a role for SETD2 in regulating cell size. SETD2 is a lysine methyltransferase and a tumor suppressor protein involved in transcription, RNA processing and DNA repair. At the molecular level, SETD2 is best known for associating with RNA polymerase II through its Set2-Rbp1 interacting (SRI) domain and methylating histone H3 on lysine 36 (H3K36) during transcription. Using multiple independent perturbation strategies, we identify SETD2 as a negative regulator of global protein synthesis rates and cell size. We provide evidence that overexpression of the H3K36 demethylase KDM4A or the oncohistone H3.3K36M also increase cell size. In addition, ectopic overexpression of a decoy SRI domain increased cell size, suggesting that the relevant substrate is engaged by SETD2 via its SRI domain. These data add a central role of SETD2 in regulating cellular physiology and warrant further studies on separating the different functions of SETD2 in cancer development.

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