Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA301681 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2932480.fastq.gz | Fastqsanger.gz | |||
| SRR2932481.fastq.gz | Fastqsanger.gz | |||
| SRR2932482.fastq.gz | Fastqsanger.gz | |||
| SRR2932483.fastq.gz | Fastqsanger.gz | |||
| SRR2932484.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Many biological processes involve post-transcriptional regulation of gene expression by alternative pre-mRNA splicing. Here, we show that an alternative splicing factor SRSF6 affects tissue homeostasis of the skin. In this dataset, we study effects on gene expression and alternative splicing upon SRSF6 overexpression (+doxycycline) in mouse skin using inducible R26-rtTA+/-, ColA1-TREtight-SRSF6+/- transgenic mice
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Project description:Many biological processes involve post-transcriptional regulation of gene expression by alternative pre-mRNA splicing. Here, we show that an alternative splicing factor SRSF6 affects tissue homeostasis of the skin. In this dataset, we study effects on gene expression and alternative splicing upon SRSF6 overexpression (+doxycycline) in mouse skin using inducible R26-rtTA+/-, ColA1-TREtight-SRSF6+/- transgenic mice 4 mixed-background strain samples (2 SRSF6-induced skin samples and 2 uninduced skin control samples)
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Project description:In the eukaryotic cell, spliceosomes assemble onto pre-mRNA cotranscriptionally. The fact that spliceosome assembly takes place in the context of a dynamic chromatin environment suggests that the state of the chromatin may affect splicing. The molecular details and mechanisms through which chromatin regulates RNA splicing, however, are still unclear. Here, we show a widespread role for the histone methyltransferase Set2 and its histone modification, H3K36 methylation, in pre-mRNA splicing through high-throughput sequencing. Moreover, we find that the effect of H3K36 methylation on pre-mRNA splicing is not dependent on changes in RNA polymerase II elongation, but are driven by the chromodomain protein Eaf3. We find that Eaf3 is recruited to intron-containing genes and that Eaf3 physically interacts with the splicing factor Prp45. Eaf3 acts with Prp45 and Prp19 after formation of the pre-catalytic B complex around the time of splicing activation revealing the step in splicing that is regulated by H3K36 methylation. These studies support a model whereby H3K36 facilitates recruitment of an “adapter protein” to support efficient, constitutive splicing.
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