LSM2-8 and XRN-2 contribute to the silencing of H3K27me3 marked genes through targeted RNA decay II
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ABSTRACT:
PROVIDER: PRJNA551255 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9602650.fastq.gz | Fastqsanger.gz | |||
| SRR9602651.fastq.gz | Fastqsanger.gz | |||
| SRR9602652.fastq.gz | Fastqsanger.gz | |||
| SRR9602643.fastq.gz | Fastqsanger.gz | |||
| SRR9602653.fastq.gz | Fastqsanger.gz |
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Project description:LSM2-8 and XRN-2 contribute to the silencing of H3K27me3 marked genes through targeted RNA decay
| PRJNA358613 | ENA
Project description:The LSM2-8 complex specifically targets nuclear RNAs generated from loci bearing histone H3K27me3 for degradation through the exonuclease XRN-2 In fission yeast and plants RNA-processing pathways including co-transcriptional degradation of nuclear mRNAs contributes to heterochromatic gene silencing additionally to the well-known transcriptional repression, but it was not knownunclear if this extra level of regulation also to occur in metazoans. Here we report the discovery of a related pathway in somatic cells of the flatworm C. elegans. The highly conserved, RNA binding LSM2-8 complex is shown to silence selectively heterochromatic reporters and endogenous genes bearing the Polycomb mark H2K27me3. LSM2-8-mediated silencing is independent of H3K9me2/me3 but depends on mes-2, the Polycomb-like histone methyl transferase. LSM2-8-mediated silencing is detectable from early embryonic stages through adulthood. The LSM2-8 complex works cooperatively with XRN-2, a 5’-3’ exonuclease, and disruption of the pathway leads to stabilized targeted mRNAs. Developmental defects and premature death were observed in worms lacking LSM-8, and levels of H3K27me3 dropped slightly at Pc-targeted loci. LSM2-8-mediated silencing of H3K27me3-bound regions defines a new mechanism of selective heterochromatin gene silencing not previously shown for higher eukaryotes.
2020-02-12 | GSE92851 | GEO
Project description:The LSM2-8 complex specifically targets nuclear RNAs generated from loci bearing histone H3K27me3 for degradation through the exonuclease XRN-2 In fission yeast and plants RNA-processing pathways including co-transcriptional degradation of nuclear mRNAs contributes to heterochromatic gene silencing additionally to the well-known transcriptional repression, but it was not knownunclear if this extra level of regulation also to occur in metazoans. Here we report the discovery of a related pathway in somatic cells of the flatworm C. elegans. The highly conserved, RNA binding LSM2-8 complex is shown to silence selectively heterochromatic reporters and endogenous genes bearing the Polycomb mark H2K27me3. LSM2-8-mediated silencing is independent of H3K9me2/me3 but depends on mes-2, the Polycomb-like histone methyl transferase. LSM2-8-mediated silencing is detectable from early embryonic stages through adulthood. The LSM2-8 complex works cooperatively with XRN-2, a 5’-3’ exonuclease, and disruption of the pathway leads to stabilized targeted mRNAs. Developmental defects and premature death were observed in worms lacking LSM-8, and levels of H3K27me3 dropped slightly at Pc-targeted loci. LSM2-8-mediated silencing of H3K27me3-bound regions defines a new mechanism of selective heterochromatin gene silencing not previously shown for higher eukaryotes.
2020-02-12 | GSE92850 | GEO
Project description:The LSM2-8 complex specifically targets nuclear RNAs generated from loci bearing histone H3K27me3 for degradation through the exonuclease XRN-2 In fission yeast and plants RNA-processing pathways including co-transcriptional degradation of nuclear mRNAs contributes to heterochromatic gene silencing additionally to the well-known transcriptional repression, but it was not knownunclear if this extra level of regulation also to occur in metazoans. Here we report the discovery of a related pathway in somatic cells of the flatworm C. elegans. The highly conserved, RNA binding LSM2-8 complex is shown to silence selectively heterochromatic reporters and endogenous genes bearing the Polycomb mark H2K27me3. LSM2-8-mediated silencing is independent of H3K9me2/me3 but depends on mes-2, the Polycomb-like histone methyl transferase. LSM2-8-mediated silencing is detectable from early embryonic stages through adulthood. The LSM2-8 complex works cooperatively with XRN-2, a 5’-3’ exonuclease, and disruption of the pathway leads to stabilized targeted mRNAs. Developmental defects and premature death were observed in worms lacking LSM-8, and levels of H3K27me3 dropped slightly at Pc-targeted loci. LSM2-8-mediated silencing of H3K27me3-bound regions defines a new mechanism of selective heterochromatin gene silencing not previously shown for higher eukaryotes.
2020-02-12 | GSE133356 | GEO
Project description:LSM2-8 and XRN-2 contribute to the silencing of H3K27me3 marked genes through targeted RNA decay I
| PRJNA358616 | ENA
Project description:ChIP-seq in wildtype and Tspyl2 loss-of-function hippocampal neurons to define H3K27me3 marked genomic regions
2018-08-21 | GSE74733 | GEO
Project description:In fission yeast and plants, RNA processing and degradation contribute to heterochromatin silencing, alongside conserved pathways of transcriptional repression. It has not been known whether similar pathways exist in metazoans. Here, we describe a pathway of silencing in Caenorhabditis elegans somatic cells, in which the highly conserved RNA-binding complex LSM2-8 contributes selectively to the repression of heterochromatic reporters and endogenous genes bearing the Polycomb mark, histone H3K27me3. This acts by degrading selected transcripts through the XRN-2 exoribonuclease. Disruption of the LSM2-8 pathway leads to mRNA stabilization. Unlike previously described pathways of heterochromatic RNA degradation, LSM2-8-mediated RNA degradation does not target nor require H3K9 methylation. Intriguingly, loss of this pathway coincides with a localized reduction in H3K27me3 at lsm-8-sensitive loci. We have thus uncovered a mechanism of RNA degradation that selectively contributes to the silencing of a subset of H3K27me3-marked genes, revealing a previously unrecognized layer of post-transcriptional control in metazoan heterochromatin.
| S-EPMC7212045 | biostudies-literature
Project description:XRN 5′-3′ exoribonucleases play crucial roles in the control of RNA processing, quality, and quantity in eukaryotes. Although genome-wide profiling of RNA decay fragments is now feasible, how XRNs shape the plant mRNA degradome remains elusive. Here, we profiled and analyzed the RNA degradomes of the Arabidopsis wild type and mutants with defects in XRN activity. Deficiency of nuclear XRN3 or cytoplasmic XRN4 but not nuclear XRN2 activity largely altered Arabidopsis mRNA decay profiles. In addition to the primary XRN4 substrates derived from decapping and microRNA-directed slicing, terminating ribosome- and exon junction complex-protected fragments produced from XRN4-mediated cytoplasmic decay also represent the most abundant decay intermediates of Arabidopsis mRNAs. Short excised linear introns and cleaved pre-mRNA fragments downstream of polyadenylation sites were polyadenylated and stabilized in the xrn3 mutant, demonstrating the function of XRN3 in the removal of cleavage remnants from pre-mRNA processing. Further analysis of stabilized XRN3 substrates confirmed that polyadenylation cleavage frequently occurs after an adenosine. An increase in decay intermediates with 5′ ends upstream of a consensus motif in the xrn4 mutant suggests an endonucleolytic cleavage mechanism targeting the 3′ untranslated region of many Arabidopsis mRNAs. However, analysis of decay fragments stabilized in the xrn4 mutant indicated that, except for microRNA-directed slicing, endonucleolytic cleavage events in the coding sequence might rarely result in major decay intermediates. Together, the results of this study reveal major substrates and products of nuclear and cytoplasmic XRNs along Arabidopsis transcripts and provide a basis for precise interpretation of RNA degradome data.
2022-09-06 | GSE205190 | GEO
Project description:Hematopoietic stem cell expansion through suppression of YTHDF2-mediated m6A-marked mRNA decay
| PRJNA422040 | ENA
Project description:We report genome-wide binding targets of REF6, a H3K27me3 demethylase and also high-throughput profiling of histone modifications of H3K27me3 in Arabidopsis flowers. Using chromatin-immunoprecipitation followed by high-throughput sequencing, we mapped thousands of binding targets of REF6 in flowers and in addition, we used a second fixative, DSG to capture more indirect targets of REF6. In order to investigate the function of indirect binding of REF6 represented H3K27me3 demethylase, the binding targets of DNA binding domain deleted REF6 were identified in the triple mutant background in which REF6 and its two homologs were mutated. Meanwhile, the H3K27me3 marked regions in both wild type and triple mutant flowers were defined. By analyzing the differentially enriched H3K27me3 region and REF6 binding profile, we found that REF6 functions to determine the boundary of H3K27me3 regions. Comparison of binding profiles of REF6 in flowers and in seedlings (ref) revealed a tissue-specific binding manner. More importantly, we found that the indirect binding of REF6 is mediated by trans factors and this indirect binding is crucial for REF6 function, especially in reproductive organs in Arabidopsis. Our results provide novel molecular insights into REF6 functions.
2018-07-09 | GSE106942 | GEO