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Effect of splicing on histone H3 K36 methylation

ABSTRACT: Histone H3 K36me3 and RNA pol II were localized by ChIP before and after inhibition of splicing by spliceostatin for 12 hr. Total matched reads for the control and SSA treated Hela samples were 11.6 and 8.2 million for anti-H3K36me3 and 6.6 and 5.0 million for anti-pol II. ChIP-seq of histone H3 K36me3 and RNA pol II in Hela cells before and after spliceosotatin treatment

ORGANISM(S): Homo sapiens

SUBMITTER: David Bentley

PROVIDER: E-GEOD-30895 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Pre-mRNA splicing is a determinant of histone H3K36 methylation.

Kim Soojin S Kim Hyunmin H Fong Nova N Erickson Benjamin B Bentley David L DL

Proceedings of the National Academy of Sciences of the United States of America 20110801 33

A chromatin code appears to mark introns and exons with distinct patterns of nucleosome enrichment and histone methylation. We investigated whether a causal relationship exists between splicing and chromatin modification by asking whether splice-site mutations affect the methylation of histone H3K36. Deletions of the 3' splice site in intron 2 or in both introns 1 and 2 of an integrated β-globin reporter gene caused a shift in relative distribution of H3K36 trimethylation away from 5' ends and t ...[more]

PMID: 21807997

Similar Datasets

Effect of splicing on histone H3 K36 methylation

Project description:Histone H3 K36me3 and RNA pol II were localized by ChIP before and after inhibition of splicing by spliceostatin for 12 hr. Total matched reads for the control and SSA treated Hela samples were 11.6 and 8.2 million for anti-H3K36me3 and 6.6 and 5.0 million for anti-pol II.

2011-09-05 | GSE30895 | GEO

Spliceostatin treatment on HeLa cells

Project description:HeLa cell line treated with Spliceostatin or methanol Three biological replicates and one technical replicate were labeled in direct and dye-swap experiments.

2011-03-08 | E-GEOD-22614 | biostudies-arrayexpress

Transcriptome changes in spliceostatin A treated cells

Project description:Pre-mRNA in eukaryotes is subjected to post-transcriptional modifications, such as capping, polyadenylation and splicing. It is well known that transcription and post-transcriptional modifications are coupled and that this coupling stimulates post-transcriptional modifications, however, the effects of post-transcriptional modifications on transcription are not fully understood. Here, we report that inhibition of U2 snRNP by a splicing inhibitor, spliceostatin A (SSA), and antisense morpholino oligonucleotide to U2 snRNA caused 3’ end down regulation in a gene-specific manner. We also show that U2 snRNP inhibition resulted in the dephosphorylation of second serine residues (Ser2) within heptad repeats of the C-terminal domain (CTD) of Pol II, which is important for transcription elongation, and this dephosphorylation was correlated with splicing inactivation. Interestingly, removal of SSA from the culture media caused restoration of the Ser2 phosphorylation and expression of the 3’ end, suggesting that transcription elongation resumed. These findings suggest that a novel checkpoint mechanism prevents pre-mRNA accumulation and the production of aberrant proteins translated from pre-mRNA upon splicing deficiencies through the dephosphorylation of CTD Ser2. Treated HeLa cells with methanol or spliceosotain A for 3 hours followed by labelling of nascent transcripts with EU for 1 hour. The EU labelled nascent RNA was purified and analyzed on human exon 1.0ST array. Three biological replicates were used for each treatment.

2013-03-28 | E-GEOD-45379 | biostudies-arrayexpress

AKT phosphorylates H3-threonine 45 to facilitate termination of gene transcription in response to DNA damage.

Project description:Purpose: In this study, we show that DNA damage-activated AKT phosphorylates threonine 45 of core histone H3 (H3-T45) Result: By genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) analysis, H3-T45 phosphorylation was distributed throughout DNA damage-responsive gene loci, particularly immediately after the transcription termination site Conclusion: AKT-mediated phosphorylation of H3-T45 regulates the processing of the 3′ end of DNA damage-activated genes to facilitate transcriptional termination MCF10A cells were ChIPed with anti-phosphorylated H3-T45, anti-phosphorylated RNA Pol II-S2 and S5, and anti-H3-K36me3.

2015-04-09 | E-GEOD-67699 | biostudies-arrayexpress

Spliceostatin treatment on HeLa cells

Project description:HeLa cell line treated with Spliceostatin or methanol

2011-03-08 | GSE22614 | GEO

Histone H3 K36me3 in wildtype, isw1 and chd1 yeast strains

Project description:ChIP-chip assays to measure the occupancy of histone H3 K36me3 over the yeast genome in wildtype, isw1 and chd1 yeast strains. ChIPs were done with K36me3 antibody (Ab 9050) in G1 arrested yeast cells.

2012-07-25 | GSE32044 | GEO

RNAseq data to study PRPF6 regulated splice forms in colon cancer cell lines

Project description:Description Alternative splicing plays critical roles in differentiation, development, and cancer. Using an integrated genomic approach, we have identified PRPF6, an RNA binding component of the pre-mRNA spliceosome, as an essential driver of oncogenesis in colon cancer. Importantly, PRPF6 is both amplified and overexpressed in colon cancer, and only colon cancer cells with high PRPF6 levels are sensitive to its loss. Our data clearly point to an important role for PRPF6 in colon cancer growth and suggest that a better understanding of its role in alternative splicing in colon cancer is warranted. To determine the specific alternative splice forms that PRPF6 regulates in colon cancer, we conducted the following experiment: Using two colon cancer cell lines (KM-12 and SW620) that have high PRPF6 levels, we inhibited PRPF6 expression using 2 independent siRNAs. We also tested the effect of U2 snRNP inhibition using both a siRNA targeting SF3B1 as well as spliceostatin A (a small molecule inhibitor of SF3B1). We then conducted RNA-seq to determine the gene expression and exonic changes that occur relative to either the non-targeting control siRNA (for siSF3B1 and siPRPF6) or the vehicle control (for spliceostatin A).

2014-05-10 | E-MTAB-2505 | biostudies-arrayexpress

Genome-wide map of Pol II and Flag-LARP7 in human HeLa cells

Project description:We generated genome-wide maps of Pol II and Flag-LARP7 in human HeLa cells. We find that Flag-LARP7 and Pol II co-locolize on Pol II-specific sn/snoRNA genes.

2017-02-02 | GSE87470 | GEO

Homo sapiens

Project description:Spliceostatin treatment on HeLa cells

| PRJNA128345 | ENA

Genome-wide map of RNA polymerase II, NELF, and DSIF in HeLa cells

Project description:Most metazoan promoters have RNA polymerase II (Pol II) paused slightly downstream of the transcription start site by NELF and DSIF. This pausing keeps these promoters available for rapid induction by P-TEFb, whose activity causes NELF to dissociate and Pol II and DSIF to elongate on the gene. ChIP-Seq data was generated for Pol II, NELF, and DSIF in HeLa cells and used to look at pausing downstream of unannotated promoters. 3x ChIP-Seq (Pol II, NELF, DSIF) in HeLa cells

2014-02-01 | E-GEOD-53008 | biostudies-arrayexpress

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