Uncoupling from transcription protects polyadenylation site cleavage from inhibition by DNA damage
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA841182 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19346928.fastq.gz | Fastqsanger.gz | |||
| SRR19346929.fastq.gz | Fastqsanger.gz | |||
| SRR19346930.fastq.gz | Fastqsanger.gz | |||
| SRR19346931.fastq.gz | Fastqsanger.gz |
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Project description:We studied the regulation of pre-messenger RNA 3'-end processing (i.e., cleavage at polyadenylation sites) in response to ultraviolet C irradiation in human cells.
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Project description:Termination of RNAPII transcription is associated with RNA 3’ end formation. For coding genes, termination is initiated by the cleavage/polyadenylation machinery. In contrast, a majority of noncoding transcription events in S. cerevisiae do not rely on RNA cleavage for termination, but instead terminate via a pathway that requires the Nrd1-Nab3-Sen1 (NNS) complex. Here we show that the S. pombe ortholog of Nrd1, Seb1, does not function in NNS-like termination, but promotes polyadenylation site selection of coding and noncoding genes. We found that Seb1 associates with 3’ end processing factors, is enriched at the 3’ end of genes, and binds RNA motifs downstream of cleavage sites. Importantly, a deficiency in Seb1 resulted in widespread changes in 3’ UTR length as a consequence of increased alternative polyadenylation. Given that Seb1 levels affected the recruitment of conserved 3’ end processing factors, our findings indicate that the conserved RNA-binding protein Seb1 co-transcriptionally controls alternative polyadenylation.
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