Surveillance of 3’ mRNA cleavage during transcription termination requires CF IB/Hrp1
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ABSTRACT:
PROVIDER: PRJNA966140 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24392720_1.fastq.gz | Fastqsanger.gz | |||
| SRR24392720_2.fastq.gz | Fastqsanger.gz | |||
| SRR24392721_1.fastq.gz | Fastqsanger.gz | |||
| SRR24392721_2.fastq.gz | Fastqsanger.gz | |||
| SRR24392722_1.fastq.gz | Fastqsanger.gz |
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Project description:CF IB/Hrp1 is part of the cleavage and polyadenylation factor (CPF) and cleavage factor (CF) complex (CPF-CF), which is responsible for 3' cleavage and maturation of pre-mRNAs. Although Hrp1 supports this process, its presence is not essential for the cleavage event. Here, we show that the main function of Hrp1 in the CPF-CF complex is the nuclear mRNA quality control of proper 3' cleavage. As such, Hrp1 acts as a nuclear mRNA retention factor that hinders transcripts from leaving the nucleus until processing is completed. Only after proper 3' cleavage, which is sensed through contacting Rna14, Hrp1 recruits the export receptor Mex67, allowing nuclear export. Consequently, its absence results in the leakage of elongated mRNAs into the cytoplasm. If cleavage is defective, the presence of Hrp1 on the mRNA retains these elongated transcripts until they are eliminated by the nuclear exosome. Together, we identify Hrp1 as the key quality control factor for 3' cleavage.
| S-EPMC10484732 | biostudies-literature
Project description:Comparison of cytoplasmic 3' elongated transcripts in hrp1-1 and wild type.
2023-09-15 | GSE231488 | GEO
Project description:Transcription termination determines the ends of transcriptional units and thereby ensures integrity of gene regulation. Here we perform genome-wide investigation of RNA polymerase II (Pol II) transcription termination in Caenorhabditis elegans and observe two distinct modes of termination. Whereas a subset of genes requires the exoribonuclease XRN2, a known termination factor, termination of other genes appears independent of, and refractory to, XRN2. Unexpectedly, promoters instruct the choice of termination mode, but XRN2-independent termination additionally requires a compatible region downstream of the 3’ end cleavage site. Hence, different termination mechanisms may affect different configurations of Pol II complexes dictated by promoters.
2018-02-05 | GSE97775 | GEO
Project description:RNAse III is an evolutionarily conserved family of endoribonuclease that cleaves dsRNA structures. Here we studied RNAse III homolog Pac1 In fission yeast to shed light on underappreciated roles of Drosha. We found that Pac1 co-transcriptional cleavage of nascent hairpin RNA structures trigger transcriptional termination by creating an entry point for “torpedo” exonucleases – that is, exonuclease that degrade the nascent RNA until they bump into the transcribing polymerases. As such termination pathway decouple termination from pre-mRNA polyadenylation, the nascent transcript are destabilized upon Pac1 cleavage, therefore expending the paradigm of post-transcriptional regulation of gene expression.
2021-02-19 | GSE167041 | GEO
Project description:RNAse III is an evolutionarily conserved family of endoribonuclease that cleaves dsRNA structures. Here we studied RNAse III homolog Pac1 In fission yeast to shed light on underappreciated roles of Drosha. We found that Pac1 co-transcriptional cleavage of nascent hairpin RNA structures trigger transcriptional termination by creating an entry point for “torpedo” exonucleases – that is, exonuclease that degrade the nascent RNA until they bump into the transcribing polymerases. As such termination pathway decouple termination from pre-mRNA polyadenylation, the nascent transcript are destabilized upon Pac1 cleavage, therefore expending the paradigm of post-transcriptional regulation of gene expression.
2021-02-19 | GSE167040 | GEO
Project description:In eukaryotes, the 3' ends of RNA polymerase II-generated transcripts are made in the majority of cases by site-specific endonucleolytic cleavage, followed by the addition of a poly(A) tail. By alternative polyadenylation, a gene can give rise to multiple mRNA isoforms that differ in the length of their 3' UTRs and hence in their susceptibility to post-transcriptional regulatory factors such as microRNAs. A series of recently conducted high-throughput studies of poly(A) site usage revealed an extensive tissue-specific control of 3’ UTR length and drastic changes in 3’ UTR length of mRNAs upon induction of proliferation in resting cells. To understand the dynamics of polyadenylation site usage, we recently identified binding sites of the major pre-mRNA 3’ end processing factors - cleavage and polyadenylation specificity factor (CPSF), cleavage stimulation factor (CstF), and cleavage factor Im (CF Im) - and mapped cleaved polyadenylation sites in HEK293 cells. Our present study extends previous findings on the role of CF Im in alternative polyadenylation and reveals that subunits of the CF Im complex generally control 3’ UTR length. More specifically, we demonstrate that the loss-of-function of CF Im68 and CF Im25 but not of CF Im59 leads to a transcriptome-wide increase of the use of proximal polyadenylation sites. 3' ends of transcripts were profiled by high-throughput sequencing in HEK 293 cells under normal conditions, and in HEK 293 cells depleted of 3' end processing factors CF Im25, CF Im59, and CF Im68.
2012-10-30 | E-GEOD-40137 | biostudies-arrayexpress
Project description:Termination is a ubiquitous phase in every transcription cycle but is incompletely understood and a subject of debate. We have used gene editing as a new approach to address its mechanism through engineered conditional depletion of the 5’-3’ exonuclease, Xrn2, or the polyadenylation signal (PAS) endonuclease, CPSF73. The ability to rapidly control Xrn2 reveals a clear and general role for it in co-transcriptional degradation of 3’ flanking region RNA and transcriptional termination. This defect is characterised genome-wide, at high resolution, using native elongating transcript sequencing (mNET-seq). An Xrn2 effect on termination requires prior RNA cleavage and we provide evidence for this by showing that catalytically inactive CPSF73 cannot restore termination to cells lacking functional CPSF73. Notably, Xrn2 plays no significant role in either Histone or snRNA gene termination even though both RNA classes undergo 3’ end cleavage. In sum, efficient termination on most protein-coding genes involves CPSF73 mediated RNA cleavage and co-transcriptional degradation of polymerase-associated RNA by Xrn2. However, as CPSF73 loss caused more extensive read-through transcription than Xrn2 elimination, it likely plays a more underpinning role in termination.
2018-02-13 | GSE109003 | GEO
Project description:Termination of RNA polymerase II (RNAPII) transcription is a fundamental step of gene expression that is critical for determining the borders between genes. In budding yeast, termination at protein-coding genes is initiated by the cleavage/polyadenylation machinery, whereas termination of most noncoding RNA (ncRNA) genes occurs via the Nrd1-Nab3-Sen1 (NNS) pathway. Unexpectedly, we show here that NNS-like transcription termination is not conserved in fission yeast. Instead, genome-wide location analyses show global recruitment of mRNA 3’ end processing factors at the end of ncRNA genes, including snoRNAs and snRNAs, and that this recruitment coincides with high levels of Ser2 and Tyr1 phosphorylation on the RNAPII C-terminal domain. We further show that termination of mRNA and ncRNA transcription requires the conserved Ysh1/CPSF-73 and Dhp1/XRN2 nucleases, supporting widespread cleavage-dependent transcription termination in fission yeast. Our findings thus reveal that a common mode of transcription termination can produce functionally and structurally distinct types of polyadenylated and non-polyadenylated RNAs.
2018-08-10 | GSE115595 | GEO
Project description:In eukaryotes, the 3' ends of RNA polymerase II-generated transcripts are made in the majority of cases by site-specific endonucleolytic cleavage, followed by the addition of a poly(A) tail. By alternative polyadenylation, a gene can give rise to multiple mRNA isoforms that differ in the length of their 3' UTRs and hence in their susceptibility to post-transcriptional regulatory factors such as microRNAs. A series of recently conducted high-throughput studies of poly(A) site usage revealed an extensive tissue-specific control of 3’ UTR length and drastic changes in 3’ UTR length of mRNAs upon induction of proliferation in resting cells. To understand the dynamics of polyadenylation site usage, we recently identified binding sites of the major pre-mRNA 3’ end processing factors - cleavage and polyadenylation specificity factor (CPSF), cleavage stimulation factor (CstF), and cleavage factor Im (CF Im) - and mapped cleaved polyadenylation sites in HEK293 cells. Our present study extends previous findings on the role of CF Im in alternative polyadenylation and reveals that subunits of the CF Im complex generally control 3’ UTR length. More specifically, we demonstrate that the loss-of-function of CF Im68 and CF Im25 but not of CF Im59 leads to a transcriptome-wide increase of the use of proximal polyadenylation sites.
2012-10-30 | GSE40137 | GEO
Project description:At the end of protein-coding genes, RNA polymerase (Pol) II undergoes a concerted transition that involves 3’-processing of the pre-mRNA and transcription termination. Here we conduct a genome-wide analysis of this 3’-transition in yeast. We find that the 3’-transition globally requires the Pol II elongation factor Spt5 and factors involved in the recognition of the poly-adenylation (pA) site and in endonucleolytic RNA cleavage. Pol II release from DNA occurs in a narrow termination window downstream of the pA site and generally requires the ‘torpedo’ exonuclease Rat1 (human XRN2). The Rat1-interacting factor Rai1 contributes to RNA degradation downstream of the pA site. Defects in the 3’-transition result in transcription interference at downstream genes, which is attenuated by a back-up termination mechanism.
2017-03-15 | GSE79222 | GEO