A NOVEL EPIGENETIC SILENCING PATHWAY INVOLVING the HIGHLY CONSERVED 5'-3' EXORIBONUCLEASE Dhp1/Rat1/Xrn2 in SCHIZOSACCHAROMYCES POMBE
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ABSTRACT:
PROVIDER: PRJNA309975 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3129010.fastq.gz | Fastqsanger.gz | |||
| SRR3129011.fastq.gz | Fastqsanger.gz | |||
| SRR3129012.fastq.gz | Fastqsanger.gz | |||
| SRR3129013.fastq.gz | Fastqsanger.gz | |||
| SRR3129009.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic gene silencing plays a critical role in regulating gene expression and contributes to organismal development and cell fate acquisition in eukaryotes. In fission yeast, Schizosaccharomyces pombe, heterochromatin-associated gene silencing is known to be mediated by RNA processing pathways including RNA interference (RNAi) and a 3’-5’ exoribonuclease complex exosome. Here, we report a new RNA-processing pathway that contributes to epigenetic gene silencing and assembly of heterochromatin mediated by 5’-3’ exoribonuclease Dhp1/Xrn2. Dhp1 mutation causes defective gene silencing both at peri-centromeric regions and at the silent mating type locus. Intriguingly, mutation of either one of two well-characterized Dhp1-interacting proteins, the Din1 pyrophosphohydrolase or the Rhn1 transcription termination factor, does not show silencing defects at the main heterochromatic regions. Dhp1 is essential in the sequential steps of establishing silencing in a manner independent of both RNAi and the exosome. Genomic and genetic analysis suggest that Dhp1 is involved in post-transcriptional silencing of repetitive regions through its catalytic activity. Our study is the first investigation into an unexpected role of Dhp1/Rat1/Xrn2 in chromatin-based silencing. These results elucidate how various RNA-processing pathways, acting together or independently, contribute to epigenetic regulation of the eukaryotic genome.
2016-01-28 | GSE77290 | GEO
Project description:Epigenetic gene silencing plays a critical role in regulating gene expression and contributes to organismal development and cell fate acquisition in eukaryotes. In fission yeast, Schizosaccharomyces pombe, heterochromatin-associated gene silencing is known to be mediated by RNA processing pathways including RNA interference (RNAi) and a 3’-5’ exoribonuclease complex exosome. Here, we report a new RNA-processing pathway that contributes to epigenetic gene silencing and assembly of heterochromatin mediated by 5’-3’ exoribonuclease Dhp1/Xrn2. Dhp1 mutation causes defective gene silencing both at peri-centromeric regions and at the silent mating type locus. Intriguingly, mutation of either one of two well-characterized Dhp1-interacting proteins, the Din1 pyrophosphohydrolase or the Rhn1 transcription termination factor, does not show silencing defects at the main heterochromatic regions. Dhp1 is essential in the sequential steps of establishing silencing in a manner independent of both RNAi and the exosome. Genomic and genetic analysis suggest that Dhp1 is involved in post-transcriptional silencing of repetitive regions through its catalytic activity. Our study is the first investigation into an unexpected role of Dhp1/Rat1/Xrn2 in chromatin-based silencing. These results elucidate how various RNA-processing pathways, acting together or independently, contribute to epigenetic regulation of the eukaryotic genome.
2016-01-28 | GSE77289 | GEO
Project description:Co-transcriptional RNA processing and surveillance factors mediate heterochromatin formation in fission yeast. In addition to RNAi, RNA elimination machinery including MTREC (Mtl1-Red1 core) and the exosome are involved in facultative heterochromatin assembly, however, the exact mechanisms remain unclear. Here we show that RNA elimination factors cooperate with the conserved exoribonuclease Dhp1/Rat1/Xrn2, which couples pre-mRNA 3â-end processing to transcription termination, to promote premature termination and facultative heterochromatin formation at meiotic genes. Dhp1 also affects termination of transcripts at genes that are targets of RNAi-mediated heterochromatin assembly. Moreover, Dhp1 facilitates constitutive heterochromatin formation and silencing at centromeric and mating-type loci. Remarkably, we find that Dhp1 interacts with the Clr4/Suv39h methyltransferase complex and acts directly to nucleate heterochromatin. Our results uncover a novel role for 3â-end processing and termination machinery in gene silencing through premature termination and suggest that non-canonical termination by Dhp1 and RNA elimination factors is linked to heterochromatin assembly. These findings have important implications for understanding mechanisms of gene silencing in higher eukaryotes. Sequencing and analysis of small RNA in two S. pombe mutants
2016-01-05 | E-GEOD-74739 | biostudies-arrayexpress
Project description:A NOVEL EPIGENETIC SILENCING PATHWAY INVOLVING the HIGHLY CONSERVED 5'-3' EXORIBONUCLEASE Dhp1/Rat1/Xrn2 in SCHIZOSACCHAROMYCES POMBE [CRAC-seq]
| PRJNA309977 | ENA
Project description:A NOVEL EPIGENETIC SILENCING PATHWAY INVOLVING the HIGHLY CONSERVED 5'-3' EXORIBONUCLEASE Dhp1/Rat1/Xrn2 in SCHIZOSACCHAROMYCES POMBE [gene expression]
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Project description:Co-transcriptional RNA processing and surveillance factors mediate heterochromatin formation in fission yeast. In addition to RNAi, RNA elimination machinery including MTREC (Mtl1-Red1 core) and the exosome are involved in facultative heterochromatin assembly, however, the exact mechanisms remain unclear. Here we show that RNA elimination factors cooperate with the conserved exoribonuclease Dhp1/Rat1/Xrn2, which couples pre-mRNA 3’-end processing to transcription termination, to promote premature termination and facultative heterochromatin formation at meiotic genes. Dhp1 also affects termination of transcripts at genes that are targets of RNAi-mediated heterochromatin assembly. Moreover, Dhp1 facilitates constitutive heterochromatin formation and silencing at centromeric and mating-type loci. Remarkably, we find that Dhp1 interacts with the Clr4/Suv39h methyltransferase complex and acts directly to nucleate heterochromatin. Our results uncover a novel role for 3’-end processing and termination machinery in gene silencing through premature termination and suggest that non-canonical termination by Dhp1 and RNA elimination factors is linked to heterochromatin assembly. These findings have important implications for understanding mechanisms of gene silencing in higher eukaryotes.
2016-01-05 | GSE74739 | GEO
Project description:We analysed the effect of depriving the human cell of the catalytic activity of the nuclear 5’ to 3’ exoribonuclease XRN2. Catalytic amino acids in this protein had been defined previously, so it was possible to design a mutated catalytically inactive form of the protein (XRN2D233A-D235A) (PMID: 19194460). We created 293 Flp-In T-REx stable cell lines that induciby silence endogenous XRN2, and concomitantly express wild-type or inactive XRN2 in fusion with EGFP at the C-terminus. Thus, complementation of silencing of endogenous XRN2 with the expression of mutant version of the protein allows to directly link potential phenotypes with the lack of XRN2 enzymatic activity. To this end we isolated total RNA from tetracycline-treated cells, depleted it from rRNA and conducted strand-specific deep sequencing.
2018-04-17 | GSE99421 | GEO
Project description:XRN2 is a conserved 5â??-->3â?? exoribonuclease that complexes with XTB-domain containing proteins. Thus, in Caenorhabditis elegans (C. elegans), the XTBD-protein PAXT-1 stabilizes XRN2 to retain its activity. XRN2 activity is also promoted by 3'(2'),5'-bisphosphate nucleotidase 1 (BPNT1) through its hydrolysis of 3â??-phosphoadenosine-5'-bisphosphate (PAP), an endogenous XRN inhibitor. Here, we find through unbiased screening that loss of bpnt-1 function suppresses lethality caused by paxt-1 deletion. This unexpected finding is explained by XRN2 autoregulation, which occurs through repression of a cryptic promoter activity and destabilization of the xrn-2 transcript. Autoregulation appears to be triggered at different thresholds of XRN2 inactivation, such that more robust XRN2 perturbation, by elimination of both PAXT-1 and BPNT1, is less detrimental to worm viability than absence of PAXT-1 alone. Like more than 15% of C. elegans genes, xrn-2 occurs in an operon, and we identify additional operons under its control, consistent with a broader function of XRN2 in polycistronic gene regulation. Regulation occurs through intercistronic regions that link genes in an operon, but similar mechanisms may allow XRN2 to operate on monocistronic genes in organisms lacking operons. Wild-type C. elegans worms were subjected to mock or xrn-2 RNAi from L1 to L4 stage at 20°C. Total RNA was extracted from the worms, and polyadenylated RNA was analyzed.
2016-08-25 | E-GEOD-79994 | biostudies-arrayexpress
Project description:XRN2 is a conserved 5’-->3’ exoribonuclease that complexes with XTB-domain containing proteins. Thus, in Caenorhabditis elegans (C. elegans), the XTBD-protein PAXT-1 stabilizes XRN2 to retain its activity. XRN2 activity is also promoted by 3'(2'),5'-bisphosphate nucleotidase 1 (BPNT1) through its hydrolysis of 3’-phosphoadenosine-5'-bisphosphate (PAP), an endogenous XRN inhibitor. Here, we find through unbiased screening that loss of bpnt-1 function suppresses lethality caused by paxt-1 deletion. This unexpected finding is explained by XRN2 autoregulation, which occurs through repression of a cryptic promoter activity and destabilization of the xrn-2 transcript. Autoregulation appears to be triggered at different thresholds of XRN2 inactivation, such that more robust XRN2 perturbation, by elimination of both PAXT-1 and BPNT1, is less detrimental to worm viability than absence of PAXT-1 alone. Like more than 15% of C. elegans genes, xrn-2 occurs in an operon, and we identify additional operons under its control, consistent with a broader function of XRN2 in polycistronic gene regulation. Regulation occurs through intercistronic regions that link genes in an operon, but similar mechanisms may allow XRN2 to operate on monocistronic genes in organisms lacking operons.
2016-08-25 | GSE79994 | GEO