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Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans

ABSTRACT: Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans

PROVIDER: PRJNA342115 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4188770.fastq.gz	Fastqsanger.gz
	SRR4188780.fastq.gz	Fastqsanger.gz
	SRR4188790.fastq.gz	Fastqsanger.gz
	SRR4188800.fastq.gz	Fastqsanger.gz
	SRR4188771.fastq.gz	Fastqsanger.gz

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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]

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

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]

2017-01-01 | GSE86513 | GEO

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]

2017-01-01 | GSE86516 | GEO

Decoupling the downstream effects of germline nuclear RNAi reveals that H3K9me3 is dispensable for heritable RNAi and the maintenance of endogenous siRNA-mediated transcriptional silencing in Caenorhabditis elegans.

Project description:Germline nuclear RNAi in C. elegans is a transgenerational gene-silencing pathway that leads to H3K9 trimethylation (H3K9me3) and transcriptional silencing at the target genes. H3K9me3 induced by either exogenous double-stranded RNA (dsRNA) or endogenous siRNA (endo-siRNA) is highly specific to the target loci and transgenerationally heritable. Despite these features, the role of H3K9me3 in siRNA-mediated transcriptional silencing and inheritance of the silencing state at native target genes is unclear. In this study, we took combined genetic and whole-genome approaches to address this question.Here we demonstrate that siRNA-mediated H3K9me3 requires combined activities of three H3K9 histone methyltransferases: MET-2, SET-25, and SET-32. set-32 single, met-2 set-25 double, and met-2 set-25;set-32 triple mutant adult animals all exhibit prominent reductions in H3K9me3 throughout the genome, with met-2 set-25;set-32 mutant worms losing all detectable H3K9me3 signals. Surprisingly, loss of high-magnitude H3K9me3 at the native nuclear RNAi targets has no effect on the transcriptional silencing state. In addition, the exogenous dsRNA-induced transcriptional silencing and heritable RNAi at oma-1, a well-established nuclear RNAi reporter gene, are completely resistant to the loss of H3K9me3.Nuclear RNAi-mediated H3K9me3 in C. elegans requires multiple histone methyltransferases, including MET-2, SET-25, and SET-32. H3K9me3 is not essential for dsRNA-induced heritable RNAi or the maintenance of endo-siRNA-mediated transcriptional silencing in C. elegans. We propose that siRNA-mediated transcriptional silencing in C. elegans can be maintained by an H3K9me3-independent mechanism.

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Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-01-01 | GSE86517 | GEO

Two H3K23 histone methyltransferases, SET-32 and SET-21, function synergistically to promote nuclear RNAi-mediated transgenerational epigenetic inheritance in Caenorhabditis elegans

Project description:Nuclear RNAi in C. elegans induces a set of transgenerationally heritable marks of H3K9me3, H3K23me3, and H3K27me3 at the target genes. The function of H3K23me3 in the nuclear RNAi pathway is largely unknown due to the limited knowledge of H3K23 histone methyltransferase (HMT). In this study we identified SET-21 as a novel H3K23 HMT. By taking combined genetic, biochemical, and genomic approaches we found that SET-21 functions synergistically with a previously reported H3K23 HMT SET-32 to deposit H3K23me3 at the native targets of germline nuclear RNAi. We identified a subset of nuclear RNAi targets that became transcriptionally activated in the set-21;set-32 double mutant. SET-21 and SET-32 are also required for a robust transgenerational gene silencing induced by exogenous dsRNA. The set-21;set-32 double mutant exhibited an enhanced mortal germline phenotype at a high temperature compared to the set-32 single mutant. Together, these results support a model in which H3K23 HMTs SET-21 and SET-32 function cooperatively to ensure the robustness of germline nuclear RNAi and promotes the germline immortality under the heat stress.

2024-12-06 | PXD052034 | Pride

ChIP-Seq of H3K9me3 and H3K36me3 after GFP or dKDM4A RNAi of S2 cells

Project description:Analysis of H3K9me3 and H3K36me3 levels in unique and repetitive regions of Drosophila genome after GFP (control) or dKDM4A RNAi of S2 cells

2018-02-15 | GSE99027 | GEO

Caenorhabditis elegans

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]

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Caenorhabditis elegans

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rnai-Transcriptomic analyses approach to identify genes associated with organ growth downstream TCTP in Arabidopsis

Project description:ra09-02_tctp - rnai - Identification of effector genes that act downstream of AtTCTP, using knockout ( tctp-2), RNAi expressing line (35S::RNAi-AtTCTP) and over expressing line (35S::AtTCTP) - transcriptome analysis in leaf of 35S::RNAi-AtTCTP versus wild type Keywords: normal vs rnai mutant comparison

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