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Alternative splicing and the epigenome in CML remission [RNA-Seq]

ABSTRACT: Alternative splicing and the epigenome in CML remission [RNA-Seq]

PROVIDER: PRJNA602827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10956600_1.fastq.gz	Fastqsanger.gz
	SRR10956600_2.fastq.gz	Fastqsanger.gz
	SRR10956601_1.fastq.gz	Fastqsanger.gz
	SRR10956601_2.fastq.gz	Fastqsanger.gz
	SRR10956602_1.fastq.gz	Fastqsanger.gz

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Alternative splicing and the epigenome in CML remission

Project description:Alternative splicing and the epigenome in CML remission

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Alternative splicing and the epigenome in CML remission [WGBS]

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Alternative splicing and the epigenome in CML remission [WGBS]

Project description:Transcriptomic and epigenomic profiling of matched CML diagnosis/remission samples revealed a reconfiguration of gene expression and DNA methylation at remission exhibiting patterns similar to those observed in healthy individuals. In contrast, alternative splicing retains chronic phase-like abnormal patterns. Most dramatic dissimilarities between remission and healthy control samples were observed in intron retention. While reduced DNA methylation around splice sites could explain increased intron retention at diagnosis, maintenance of high intron retention levels at remission has other causes, such as reduced splicing factor expression and histone modifications.

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Alternative splicing and the epigenome in CML remission [RNA-Seq]

2020-06-30 | GSE144119 | GEO

Alternative splicing and the epigenome in CML remission

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

2020-12-19 | GSE163527 | GEO

Chromatin-mediated alternative splicing regulates cocaine reward behavior

Project description:Neuronal alternative splicing is a key gene regulatory mechanism in brain. Yet the spliceosome machinery is insufficient to fully specify splicing complexity. In considering the role of the epigenome in activity-dependent alternative splicing, we and others find the histone modification, H3K36me3, to be a putative splicing regulator. In the current study, we found that mouse cocaine self-administration caused widespread differential alternative splicing, concomitant with enrichment of H3K36me3 at differentially spliced junctions. Importantly, only targeted epigenetic editing can distinguish between a direct role of H3K36me3 in splicing and an indirect role via regulation of splice factor expression elsewhere on the genome. We targeted Srsf11, which was both alternatively spliced and H3K36me3 enriched in brain following cocaine self-administration. Results: Epigenetic editing of H3K36me3 at Srsf11 was sufficient to drive its alternative splicing and enhanced cocaine self-administration, establishing the direct causal relevance of H3K36me3 to alternative splicing of Srsf11 and to reward behavior.

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Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB

Project description:This SuperSeries is composed of the following subset Series: GSE23513: Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (HJAY) GSE23514: Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (Exon array) Refer to individual Series

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Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns

Project description:Alternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects. HeLa cell line was stably transfected with shRNA plasmids targeting CstF64. Total RNA was isolated from CstF64 KD cells and wild-type control cells using Trizol according to manufacturerâs protocols. Samples were deep sequenced in duplicate using the Illumina GAIIx system.

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Project description:We analyzed alternative splicing with Shh medulloblastoma. This dataset contains bam files of whole genome sequencing from 4 cases. Genomic DNA was isolated from both tumor and matched control specimens. We performed whole genome sequence on Illumina Hiseq.

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Regulation of alternative splicing by histone modifications

Project description:Alternative splicing of pre-mRNA is a prominent mechanism to generate protein diversity, yet its regulation is poorly understood. Here, we demonstrate a direct role for histone modifications in alternative splicing. We find distinctive histone modification signatures which correlate with splicing outcome in a set of human genes. Modulation of histone modifications causes splice site switching. The mechanism for histone-mediated splice site selection involves a histone mark which is read by a chromatin protein, which in turn recruits a splicing regulator. These results outline an adaptor system for reading of histone marks by the pre-mRNA splicing machinery. To obtain an estimate of how many PTB-dependent alternative splicing events are regulated by SET2/MRG15-mediated recruitment of PTB, we carried out a genomewide comparative analysis of alternative splicing in hMSC cells depleted of either SETD2, MRG15 or PTB using specific siRNAs, or mock-depleted using a control siRNA.

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