Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA342125 | ENA |
REPOSITORIES: ENA
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Project description:Germline nuclear RNAi in C. elegans is a transgenerational gene-silencing pathway that leads to the H3K9 trimethylation (H3K9me3) response and transcriptional repression of target genes. The H3K9me3 response induced either by exogenous dsRNA or endogenous siRNA (endo-siRNA) is highly specific to the target loci and transgenerationally heritable. Despite these features, the role of H3K9me3 in transcriptional repression and heritable gene silencing at native target genes has not been tested. To resolve this gap, we first determined that the combined activities of three H3K9 histone methyltransferases (HMTs), MET-2, SET-25, and SET-32, are responsible for virtually all of the detectable level of germline nuclear RNAi-dependent H3K9me3 at native genes, triggered either by exogenous dsRNA or endo-siRNAs. By performing RNA Polymerase II ChIP-seq and pre-mRNA-seq analyses, we found that the loss of the H3K9me3 response at germline nuclear RNAi targets in the met-2;set-25;set-32 mutant does not lead to any defect in transcriptional repression or heritable RNAi. Therefore, H3K9me3 is not required for exogenous dsRNA-induced heritable RNAi or the maintenance of endo siRNA-mediated transcriptional silencing in C. elegans germline. This study provides a unique paradigm in which transcriptional silencing and heterochromatin, triggered by the same upstream pathway, can be decoupled.
2017-01-01 | GSE86513 | GEO
Project description:Germline nuclear RNAi in C. elegans is a transgenerational gene-silencing pathway that leads to the H3K9 trimethylation (H3K9me3) response and transcriptional repression of target genes. The H3K9me3 response induced either by exogenous dsRNA or endogenous siRNA (endo-siRNA) is highly specific to the target loci and transgenerationally heritable. Despite these features, the role of H3K9me3 in transcriptional repression and heritable gene silencing at native target genes has not been tested. To resolve this gap, we first determined that the combined activities of three H3K9 histone methyltransferases (HMTs), MET-2, SET-25, and SET-32, are responsible for virtually all of the detectable level of germline nuclear RNAi-dependent H3K9me3 at native genes, triggered either by exogenous dsRNA or endo-siRNAs. By performing RNA Polymerase II ChIP-seq and pre-mRNA-seq analyses, we found that the loss of the H3K9me3 response at germline nuclear RNAi targets in the met-2;set-25;set-32 mutant does not lead to any defect in transcriptional repression or heritable RNAi. Therefore, H3K9me3 is not required for exogenous dsRNA-induced heritable RNAi or the maintenance of endo siRNA-mediated transcriptional silencing in C. elegans germline. This study provides a unique paradigm in which transcriptional silencing and heterochromatin, triggered by the same upstream pathway, can be decoupled.
2017-01-01 | GSE86515 | GEO
Project description:Germline nuclear RNAi in C. elegans is a transgenerational gene-silencing pathway that leads to the H3K9 trimethylation (H3K9me3) response and transcriptional repression of target genes. The H3K9me3 response induced either by exogenous dsRNA or endogenous siRNA (endo-siRNA) is highly specific to the target loci and transgenerationally heritable. Despite these features, the role of H3K9me3 in transcriptional repression and heritable gene silencing at native target genes has not been tested. To resolve this gap, we first determined that the combined activities of three H3K9 histone methyltransferases (HMTs), MET-2, SET-25, and SET-32, are responsible for virtually all of the detectable level of germline nuclear RNAi-dependent H3K9me3 at native genes, triggered either by exogenous dsRNA or endo-siRNAs. By performing RNA Polymerase II ChIP-seq and pre-mRNA-seq analyses, we found that the loss of the H3K9me3 response at germline nuclear RNAi targets in the met-2;set-25;set-32 mutant does not lead to any defect in transcriptional repression or heritable RNAi. Therefore, H3K9me3 is not required for exogenous dsRNA-induced heritable RNAi or the maintenance of endo siRNA-mediated transcriptional silencing in C. elegans germline. This study provides a unique paradigm in which transcriptional silencing and heterochromatin, triggered by the same upstream pathway, can be decoupled.
2017-01-01 | GSE86516 | GEO
Project description:Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans
| PRJNA342115 | ENA
Project description:Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans [RNA-seq]
| PRJNA342126 | ENA
Project description:Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans [ChIP-seq]
| PRJNA342127 | ENA
Project description:The germline is an immortal cell lineage and therefore must accurately transmit genetic and epigenetic information over infinite cell divisions to ensure fertility and species survival. Endogenous siRNAs (endo-siRNAs), which are highly expressed in the parental germline and inherited in their progeny, represent one mechanism by which epigenetic information can be transmitted from one generation to the next. In C. elegans, this is accomplished by the nuclear RNAi pathway, which ensures robust inheritance of endo-siRNAs and of target gene silencing through deposition of H3K9me3 marks at target loci. How these marks are maintained in subsequent generations is unknown. Here, we show that the C. elegans micro-orchidia homolog, MORC-1, functions downstream of endo-siRNAs to mediate target silencing and maintenance of siRNA-dependent H3K9me3 marks. Like the established members of the nuclear RNAi pathway, morc-1 is essential for germline maintenance and thus morc-1(-) mutants exhibit a mortal germline phenotype. Furthermore, morc-1(-) mutants exhibit severe decondensation of germline chromatin. Through a forward genetic screen, we have identified mutations in the gene encoding MET-1, a H3K36 histone methyltransferase, that potently suppress morc-1(-) germline mortality. We show that morc-1(-) mutants exhibit progressive, met-1-dependent enrichment of H3K36me3 and that mutation of met-1 can restore germline chromatin organization in late generation morc-1(-) mutants. Our data suggest that MORC-1 is required to repress MET-1 activity at nuclear RNAi target genes and that in the absence of this repression, MET-1-mediated encroachment of euchromatin leads to detrimental decondensation of germline chromatin and germline mortality.
2017-05-22 | GSE89887 | GEO
Project description:dsRNA-mediated gene silencing (RNAi) can be inherited for multiple generations in C. elegans. To understand this process we conducted a genetic screen for animals defective for transmitting RNAi silencing signals to future generations. This screen identified the gene heritable RNAi defective (hrde)-1. hrde-1 encodes an Argonaute (Ago) that associates with siRNAs in germ cells of the progeny of animals exposed to dsRNA. In nuclei of these germ cells, HRDE-1 engages the Nrde nuclear RNAi pathway to promote RNAi inheritance, and directs H3K9me3 chromatin marks at RNAi targeted genomic loci. Under normal growth conditions, HRDE-1 associates with endogenously expressed small RNAs, which direct nuclear gene silencing in germ cells. In RNAi inheritance mutant animals, silencing is lost over generational time. Concurrently, RNAi inheritance mutant animals exhibit progressively worsening germline defects that ultimately lead to sterility. These results establish that the Ago HRDE-1 directs gene-silencing events in germ cell nuclei, which are required for multi-generational RNAi inheritance and immortality of the germ cell lineage. We propose that C. elegans use the RNAi inheritance machinery to transmit epigenetic information, accrued by past generations, into future generations to ensure immortality of the germ cell lineage. H3K9me3 Chip-IP for C. elegans strains nrde-3, nrde-4, glp-4. Small RNA-seq for small RNAs co-immunoprecipitated with HRDE-1
2012-07-30 | E-GEOD-38041 | biostudies-arrayexpress
Project description:RNA interference (RNAi) is a conserved gene silencing process that exists in diverse organisms to protect genome integrity and regulate gene expression. In C. elegans, the majority of RNAi pathway proteins localize to perinuclear, phase-separated germ granules, which are comprised of sub-domains referred to as P granules, Mutator foci, Z granules, and SIMR foci. However, the protein components and function of the newly discovered SIMR foci are unknown. Here we demonstrate that HRDE-2 localizes to SIMR foci and interacts with the germline nuclear RNAi Argonaute HRDE-1. Furthermore, HRDE-1 also localizes to SIMR foci, dependent on HRDE-2, but only in its small RNA unbound state. This germ granule localization is critical to promote the small RNA binding specificity of HRDE-1 and, in the absence of HRDE-2, HRDE-1 exclusively loads CSR-class 22G-RNAs rather than WAGO-class 22G-RNAs, resulting in H3K9me3 deposition on CSR-target genes. Thus, our study demonstrates that HRDE-2 is critical to ensure that the correct small RNAs are used to guide nuclear RNA silencing in the C. elegans germline.
2023-07-27 | MSV000092546 | MassIVE
Project description:dsRNA-mediated gene silencing (RNAi) can be inherited for multiple generations in C. elegans. To understand this process we conducted a genetic screen for animals defective for transmitting RNAi silencing signals to future generations. This screen identified the gene heritable RNAi defective (hrde)-1. hrde-1 encodes an Argonaute (Ago) that associates with siRNAs in germ cells of the progeny of animals exposed to dsRNA. In nuclei of these germ cells, HRDE-1 engages the Nrde nuclear RNAi pathway to promote RNAi inheritance, and directs H3K9me3 chromatin marks at RNAi targeted genomic loci. Under normal growth conditions, HRDE-1 associates with endogenously expressed small RNAs, which direct nuclear gene silencing in germ cells. In RNAi inheritance mutant animals, silencing is lost over generational time. Concurrently, RNAi inheritance mutant animals exhibit progressively worsening germline defects that ultimately lead to sterility. These results establish that the Ago HRDE-1 directs gene-silencing events in germ cell nuclei, which are required for multi-generational RNAi inheritance and immortality of the germ cell lineage. We propose that C. elegans use the RNAi inheritance machinery to transmit epigenetic information, accrued by past generations, into future generations to ensure immortality of the germ cell lineage.
2012-07-30 | GSE38041 | GEO