Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA338699 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4020850_1.fastq.gz | Fastqsanger.gz | |||
| SRR4020850_2.fastq.gz | Fastqsanger.gz | |||
| SRR4020851_1.fastq.gz | Fastqsanger.gz | |||
| SRR4020851_2.fastq.gz | Fastqsanger.gz | |||
| SRR4020852_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 20 |
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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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Project description:This study investigated the role Rtf2 plays on the replication fork barrier (RFB) activity of RTS1 in S. pombe. We confirm Rtf2 is important for the full barrier activity of the RTS1-Rtf1 RFB. We show that Rtf2 does not enact its enhancing effect on RTS1 RFB activity via binding to Region A of RTS1, but instead we find it to be closely associated with several splicing factors. Analysis of cells deleted for rtf2 by cDNA-Seq reveal splicing defects specifically effecting intron retention, including for the Rtf1 transcript. We show that intron retention within rtf1 is responsible for the reduced barrier activity of RTS1 when rtf2 is deleted. This study reveals Rtf2 to be an important factor for maintaining efficient splicing within the cell.
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Project description:This study investigated the role Rtf2 plays on the replication fork barrier (RFB) activity of RTS1 in S. pombe. We confirm Rtf2 is important for the full barrier activity of the RTS1-Rtf1 RFB. We show that Rtf2 does not enact its enhancing effect on RTS1 RFB activity via binding to Region A of RTS1, but instead we find it to be closely associated with several splicing factors. Analysis of cells deleted for rtf2 by cDNA-Seq reveal splicing defects specifically effecting intron retention, including for the Rtf1 transcript. We show that intron retention within rtf1 is responsible for the reduced barrier activity of RTS1 when rtf2 is deleted. This study reveals Rtf2 to be an important factor for maintaining efficient splicing within the cell.
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