Caenorhabditis elegans
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PROVIDER: PRJNA342127 | ENA |
REPOSITORIES: ENA
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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 [pre-mRNA-seq]
| PRJNA342125 | 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
| PRJNA342115 | ENA
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: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 | GSE86513 | GEO
Project description:Small RNA-guided chromatin silencing, also referred to as nuclear RNAi, plays an essential role in genome surveillance in eukaryotes and provides a unique paradigm to explore the complexity in RNA-mediated chromatin regulation and transgenerational epigenetics. A well-recognized paradox in this research area is that transcription of the target loci is necessary for the initiation and maintenance of the silencing at the same loci. How the two opposing activities (transcriptional activation and repression) are coordinated during animal development is poorly understood. To resolve this gap, we took single-molecule RNA imaging, deep-sequencing, and genetic approaches towards delineating the developmental regulation and subcellular localization of RNA transcripts of two exemplary endogenous germline nuclear RNAi targets in C. elegans, Cer3 and Cer8 LTR retrotransposons. By examining the wild type and a collection of mutant strains, we found that transcription and silencing cycle of Cer3 and Cer8 is tightly coupled with the early embryogenesis and germline mitotic and meiotic cell cycles. Strikingly, Cer3 and Cer8 transcripts are exclusively localized in the nuclei of germ cells in both wild type and germline nuclear RNAi-defective mutant animals. RNA-sequencing analysis found that this nuclear enrichment feature is a general feature for the endogenous targets of the germline nuclear RNAi pathway. In addition, the germline and somatic repressions of Cer3 have different genetic requirement for the three H3K9 histone methyltransferases, MET-2, SET-25, and SET-32, in conjunction with the nuclear Argonaute protein WAGO-9/HRDE-1. These results provide a first comprehensive cellular and developmental characterization of the nuclear RNAi-targeted endogenous targets throughout animal reproductive cycle. Altogether, these results support a model in which (1) both the transcriptional activation and repression steps of the germline nuclear RNAi pathway are tightly coupled with animal development, (2) the endogenous targets exhibit a hallmark of nuclear enrichment of their transcripts, and (3) different heterochromatin enzymes play distinct roles in somatic and germline silencing of the endogenous targets.
2018-08-11 | GSE118428 | GEO
Project description:Small RNA-guided chromatin silencing, also referred to as nuclear RNAi, plays an essential role in genome surveillance in eukaryotes and provides a unique paradigm to explore the complexity in RNA-mediated chromatin regulation and transgenerational epigenetics. A well-recognized paradox in this research area is that transcription of the target loci is necessary for the initiation and maintenance of the silencing at the same loci. How the two opposing activities (transcriptional activation and repression) are coordinated during animal development is poorly understood. To resolve this gap, we took single-molecule RNA imaging, deep-sequencing, and genetic approaches towards delineating the developmental regulation and subcellular localization of RNA transcripts of two exemplary endogenous germline nuclear RNAi targets in C. elegans, Cer3 and Cer8 LTR retrotransposons. By examining the wild type and a collection of mutant strains, we found that transcription and silencing cycle of Cer3 and Cer8 is tightly coupled with the early embryogenesis and germline mitotic and meiotic cell cycles. Strikingly, Cer3 and Cer8 transcripts are exclusively localized in the nuclei of germ cells in both wild type and germline nuclear RNAi-defective mutant animals. RNA-sequencing analysis found that this nuclear enrichment feature is a general feature for the endogenous targets of the germline nuclear RNAi pathway. In addition, the germline and somatic repressions of Cer3 have different genetic requirement for the three H3K9 histone methyltransferases, MET-2, SET-25, and SET-32, in conjunction with the nuclear Argonaute protein WAGO-9/HRDE-1. These results provide a first comprehensive cellular and developmental characterization of the nuclear RNAi-targeted endogenous targets throughout animal reproductive cycle. Altogether, these results support a model in which (1) both the transcriptional activation and repression steps of the germline nuclear RNAi pathway are tightly coupled with animal development, (2) the endogenous targets exhibit a hallmark of nuclear enrichment of their transcripts, and (3) different heterochromatin enzymes play distinct roles in somatic and germline silencing of the endogenous targets.
2018-08-11 | GSE118379 | GEO
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:Gene silencing mediated by dsRNA (RNAi) can persist for multiple generations in C. elegans (termed RNAi inheritance). Here we describe the results of a forward genetic screen in C. elegans that has identified six factors required for RNAi inheritance: GLH-1/VASA, PUP-1/CDE-1, MORC-1, SET-32, and two novel nematode-specific factors that we term here (heritable RNAi defective) HRDE-2 and HRDE-4. The new RNAi inheritance factors exhibit mortal germline (Mrt) phenotypes, which we show is likely caused by epigenetic deregulation in germ cells. We also show that HRDE-2 contributes to RNAi inheritance by facilitating the binding of small RNAs to the inheritance Argonaute (Ago) HRDE-1. Together, our results identify additional components of the RNAi inheritance machinery whose sequence conservation provides insights into the molecular mechanism of RNAi inheritance, further our understanding of how the RNAi inheritance machinery promotes germline immortality, and show that HRDE-2 couples the inheritance Ago HRDE-1 with the small RNAs it needs to direct RNAi inheritance and germline immortality.
2017-06-20 | GSE92840 | GEO