Germline- and soma-specific heritable epigenetic silencing at an endogenous locus
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ABSTRACT:
PROVIDER: PRJNA322336 | ENA |
REPOSITORIES: ENA
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Project description:The emergence and transmission of epigenetic signals across generations can quickly and efficiently alter gene expression in a population. We describe an epigenetic silencing signal whose initiation, transmission properties, genetic requirements and site of action are distinct from previously described epigenetic inheritance in C. elegans. A multi-copy transgene containing the region upstream of sid-1 silences sid-1 and upstream genes. Once established, silencing is stable in the absence of the array and can be maintained without selection for 13 generations. We show that the silenced state can be transmitted to progeny in the absence of the silenced locus, but that inherited silencing is dependent on the nuclear RNAi Argonaute HRDE-1, which stabilizes silencing siRNAs that target sid-1 exons. Notably, at each generation, the RNAi-dependent germline silenced sid-1 locus transitions to a chromatin-dependent silenced state in somatic cells, indicating that the mechanisms of transgenerational silencing in the soma and germline are distinct.
2017-02-16 | GSE81707 | GEO
Project description:The emergence and transmission of epigenetic signals across generations can quickly and efficiently alter gene expression in a population. We describe an epigenetic silencing signal whose initiation, transmission properties, genetic requirements and site of action are distinct from previously described epigenetic inheritance in C. elegans. A multi-copy transgene containing the region upstream of sid-1 silences sid-1 and upstream genes. Once established, silencing is stable in the absence of the array and can be maintained without selection for 13 generations. We show that the silenced state can be transmitted to progeny in the absence of the silenced locus, but that inherited silencing is dependent on the nuclear RNAi Argonaute HRDE-1, which stabilizes silencing siRNAs that target sid-1 exons. Notably, at each generation, the RNAi-dependent germline silenced sid-1 locus transitions to a chromatin-dependent silenced state in somatic cells, indicating that the mechanisms of transgenerational silencing in the soma and germline are distinct.
2017-02-16 | GSE81706 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-02-16 | GSE81708 | GEO
Project description:The importance of transgenerationally inherited epigenetic states to organismal fitness remains unknown as well-documented examples are often not amenable to mechanistic analysis or rely on artificial reporter loci. Here we describe an induced silenced state at an endogenous locus that persists, at 100% transmission without selection, for up to 13 generations. This unusually persistent silencing enables a detailed molecular genetic analysis of an inherited epigenetic state. We find that silencing is dependent on germline nuclear RNAi factors and post-transcriptional mechanisms. Consistent with these later observations, inheritance does not require the silenced locus, and we provide genetic evidence that small RNAs embody the inherited silencing signal. Notably, heritable germline silencing directs somatic epigenetic silencing. Somatic silencing does not require somatic nuclear RNAi but instead requires both maternal germline nuclear RNAi and chromatin-modifying activity. Coupling inherited germline silencing to somatic silencing may enable selection for physiologically important traits.
| S-EPMC5389115 | biostudies-literature
Project description:Drosophila TRAP soma vs germline
| PRJNA961150 | ENA
Project description:To define what genes are predominantly or specifically expressed in either soma or germline in C. elegans adults, total RNA was extracted from germline-less glp-4 mutant animals or from dissected gonads, respectively. Total RNA sequencing was peformed in duplicates. Four samples in total.
2015-01-08 | E-GEOD-62857 | biostudies-arrayexpress
Project description:To define what genes are predominantly or specifically expressed in either soma or germline in C. elegans adults, total RNA was extracted from germline-less glp-4 mutant animals or from dissected gonads, respectively.
2015-01-08 | GSE62857 | 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: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