Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144241 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR315684.fastq.gz | Fastqsanger.gz |
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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
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.
2011-07-25 | GSE30902 | GEO
Project description:Setd2 catalyzes trimethylation of lysine 36 on histone H3. H3K36me3 is deposited mainly in the gene body and has recently been demonstrated to play a role in regulating transcriptional elongation and alternative splicing. We conduct deep sequencing in 2-month old control (APCmin) and APCmin; Setd2IEC-/- mice intestinal cells to understand the splicing events regulated by Setd2.
2017-09-01 | GSE95663 | GEO
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
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
Project description:The dysregulation of the histone H3 lysine 36 (H3K36) methyltransferase, SETD2, is associated with worse clinical outcomes and metastasis in clear cell Renal Cell Carcinoma (ccRCC). Here, we reveal that kidney cancer cells displaying diminished H3K36me3 levels (SETD2 deficiency) show increased sensitivity to the anti-tumor effects of the DNA hypomethylating agent 5-aza-2’-deoxycytidine (Decitabine/DAC). DAC treatment induced stronger viral mimicry activation and immunostimulatory signals by higher transposable element (TE) expression in SETD2-mutant cancer cells. Surprisingly, we demonstrate that the increased TE abundance in SETD2-knockout (SETD2-KO) kidney cancer cells is substantially derived from mis-spliced products induced by DAC treatment. Epigenetic profiling suggests that differential DNA methylation, H3K36me3, and H3K9me3 marks across exons and intronic TEs might contribute to elevated mis-splicing rates specifically in the SETD2 loss context. Finally, SETD2 dysregulation also sensitized tumors in vivo to combinatorial therapy of DAC and immune checkpoint inhibitors highlighting the translational potential for this precision medicine.
2023-01-27 | GSE198673 | GEO
Project description:The dysregulation of the histone H3 lysine 36 (H3K36) methyltransferase, SETD2, is associated with worse clinical outcomes and metastasis in clear cell Renal Cell Carcinoma (ccRCC). Here, we reveal that kidney cancer cells displaying diminished H3K36me3 levels (SETD2 deficiency) show increased sensitivity to the anti-tumor effects of the DNA hypomethylating agent 5-aza-2’-deoxycytidine (Decitabine/DAC). DAC treatment induced stronger viral mimicry activation and immunostimulatory signals by higher transposable element (TE) expression in SETD2-mutant cancer cells. Surprisingly, we demonstrate that the increased TE abundance in SETD2-knockout (SETD2-KO) kidney cancer cells is substantially derived from mis-spliced products induced by DAC treatment. Epigenetic profiling suggests that differential DNA methylation, H3K36me3, and H3K9me3 marks across exons and intronic TEs might contribute to elevated mis-splicing rates specifically in the SETD2 loss context. Finally, SETD2 dysregulation also sensitized tumors in vivo to combinatorial therapy of DAC and immune checkpoint inhibitors highlighting the translational potential for this precision medicine.
2023-01-27 | GSE198670 | GEO
Project description:Epigenetic regulation of gene expression through histone modifications like methylation of various lysine residues are essential for embryonic development. Here we removed SETD2, a methyltransferase for histone 3 lysine 36 trimethylation (H3K36me3), in the developing dorsal forebrain in mice and show it is required for proper area patterning (arealization) of the neocortex and the formation of thalamo-cortico-thalamic circuits by maintaining the expression of clustered protocadherin (Pcdh) genes in an H3K36me3 methyltransferase-dependent manner. Moreover, the Setd2 mutant mice exhibit defects in social interaction, motor endurance and spatial memory, reminiscent of patients with the Sotos-like syndrome bearing SETD2 mutations.
2020-10-01 | GSE138153 | GEO
Project description:Epigenetic regulation of gene expression through histone modifications like methylation of various lysine residues are essential for embryonic development. Here we removed SETD2, a methyltransferase for histone 3 lysine 36 trimethylation (H3K36me3), in the developing dorsal forebrain in mice and show it is required for proper area patterning (arealization) of the neocortex and the formation of thalamo-cortico-thalamic circuits by maintaining the expression of clustered protocadherin (Pcdh) genes in an H3K36me3 methyltransferase-dependent manner. Moreover, the Setd2 mutant mice exhibit defects in social interaction, motor endurance and spatial memory, reminiscent of patients with the Sotos-like syndrome bearing SETD2 mutations.
2020-09-30 | GSE137622 | GEO
Project description:SETD2 is one of most frequently mutated genes in renal cell carcinoma. It is generally known as the only histone methyltransferase that catalyze the trimethylation of lysine 36 on histone H3 (H3K36me3). Mutation of this gene and/or loss of its mark have been linked to metastasis and worse patient outcomes in kidney cancer. In this paper, we will examine the mechanism by which SETD2 loss induces epithelial-to-mesenchymal transition (EMT), which is a major pathway that drives invasion and early metastasis in various cancer types. To achieve the goals, we performed several omics analysis including RNA-seq, ChIP-seq and ATAC-seq to characterize how SETD2 deletion alters transcriptome and epigenome.
2023-07-12 | GSE213258 | GEO