Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA293216 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2171450.fastq.gz | Fastqsanger.gz | |||
| SRR2171441.fastq.gz | Fastqsanger.gz | |||
| SRR2171451.fastq.gz | Fastqsanger.gz | |||
| SRR2171442.fastq.gz | Fastqsanger.gz | |||
| SRR2171452.fastq.gz | Fastqsanger.gz |
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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.
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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).
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