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CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [ChIP-Seq]

ABSTRACT: The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31485 | GEO | 2011/10/06

SECONDARY ACCESSION(S): PRJNA154051

REPOSITORIES: GEO

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CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq]

2011-10-06 | GSE31486 | GEO

CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq]

Project description:The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons. CTCF ChIP-seq was performed in BJAB and BL41 B cell lines and normalized relative to Rabbit Ig control IP-seq reads. RNA-seq was performed in BJAB and BL41 cells transduced with shRNA against CTCF or RFP as a control, and in untransduced cells as well.

2011-10-06 | E-GEOD-31486 | biostudies-arrayexpress

CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [ChIP-Seq]

2011-10-06 | E-GEOD-31485 | biostudies-arrayexpress

Effects of dynamic cytosine methylation on alternative pre-mRNA splicing in T lymphocytes

Project description:Intragenic 5-methylcytosine and CTCF mediate opposing affects on pre-mRNA splicing: CTCF promotes inclusion of weak upstream exons through RNA polymerase II pausing, whereas 5-methylcytosine evicts CTCF, leading to exon exclusion. However, the mechanisms governing dynamic DNA methylation at CTCF binding sites were unclear. In this study, we identify the methylcytosine dioxygenases TET1 and TET2 as active regulators of CTCF-mediated alternative splicing through conversion of 5-methylcytosine to its oxidation derivatives.

2016-01-04 | GSE74850 | GEO

Effects of dynamic cytosine methylation on alternative pre-mRNA splicing in T lymphocytes

2016-01-04 | E-GEOD-74850 | biostudies-arrayexpress

CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing

Project description:This SuperSeries is composed of the following subset Series: GSE31485: CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [ChIP-Seq] GSE31486: CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq] Refer to individual Series

2011-10-05 | E-GEOD-31278 | biostudies-arrayexpress

CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing

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

2011-10-06 | GSE31278 | GEO

CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing.

Project description:Alternative splicing of pre-messenger RNA is a key feature of transcriptome expansion in eukaryotic cells, yet its regulation is poorly understood. Spliceosome assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence alternative splicing. Supporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at exons relative to introns. Moreover, the rate of transcription elongation has been linked to alternative splicing. Here we provide the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide. We further show that CTCF binding to CD45 exon 5 is inhibited by DNA methylation, leading to reciprocal effects on exon 5 inclusion. These findings provide a mechanistic basis for developmental regulation of splicing outcome through heritable epigenetic marks.

| S-EPMC7398428 | biostudies-literature

An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis

Project description:CTCF plays key roles in gene regulation, chromatin insulation, imprinting, X chromosome inactivation and organizing the higher-order chromatin architecture of mammalian genomes. Previous studies have mainly focused on the roles of the canonical CTCF isoform. Here, we explore the functions of an alternatively spliced human CTCF isoform in which exons 3 and 4 are skipped, producing a shorter isoform (CTCF-s). Functionally, we find that CTCF-s competes with the genome binding of canonical CTCF and binds a similar DNA sequence. CTCF-s binding disrupts CTCF/cohesin binding, alters CTCF-mediated chromatin looping and promotes the activation of IFI6 that leads to apoptosis. This effect is caused by an abnormal long-range interaction at the IFI6 enhancer and promoter. Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.

2019-01-12 | GSE108869 | GEO

Alternative Splicing in Erythropoiesis

Project description:Differentiating erythroid cells execute a unique gene expression program that insures synthesis of the appropriate proteome at each stage of maturation. Standard expression microarrays provide important insight into erythroid gene expression, but cannot detect qualitative changes in transcript structure, mediated by RNA processing, that alter structure and function of encoded proteins. We analyzed stage-specific changes in the late erythroid transcriptome via use of high resolution microarrays that detect altered expression of individual exons. Ten differentiation-associated changes in erythroblast splicing patterns were identified, including the previously known activation of protein 4.1R exon 16 splicing. Six new alternative splicing switches involving enhanced inclusion of internal cassette exons were discovered, as well as three changes in use of alternative first exons. All of these erythroid stage-specific splicing events represent activated inclusion of authentic annotated exons, suggesting they represent an active regulatory process rather than a general loss of splicing fidelity. The observation that three of the regulated transcripts encode RNA binding proteins (SNRP70, HNRPLL, MBNL2) may indicate significant changes in the RNA processing machinery of late erythroblasts. Together these results support the existence of a regulated alternative pre-mRNA splicing program that is critical for late erythroid differentiation. Keywords: Time course; Splicing-sensitive microarray

2009-07-01 | GSE14588 | GEO

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