Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248734 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1301070.fastq.gz | Fastqsanger.gz | |||
| SRR1301080.fastq.gz | Fastqsanger.gz | |||
| SRR1301071.fastq.gz | Fastqsanger.gz | |||
| SRR1301081.fastq.gz | Fastqsanger.gz | |||
| SRR1301072.fastq.gz | Fastqsanger.gz |
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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: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:We describe the identification and characterization of genomic regions that are targeted by germline nuclear RNAi in C. elegans for transcriptional silencing and heterochromatic response.
2015-01-01 | GSE58031 | GEO
Project description:Histone H3 lysine 9 methylation (H3K9me) and nuclear RNAi are two processes with roles in repression of repetitive elements and regulation of gene expression. Recently, they were also implicated in dosage compensation, a mechanism that accommodates for the differences in gene dosage between the biological sexes. In Caenorhabditis elegans, dosage compensation is achieved via epigenetic modifications on both X chromosomes of hermaphrodites, effectively dampening their expression by half to match the single X chromosome in males. This chromosome-wide process also relies on the anchoring and compaction of the X chromosomes near the nuclear lamina, mediated by the H3K9 histone methyltransferases MET-2, SET-25 and SET-32. H3K9me is also involved in gene silencing during nuclear RNAi, and recent evidence suggests that mutations in the nuclear RNAi machinery impact X chromosome compaction and dosage compensation. The nuclear Argonautes HRDE-1 and NRDE-3 are responsible for the recruitment of the H3K9 histone methyltransferases to targets in the germline and the soma, respectively, during nuclear RNAi. We investigated the impact of the loss of nuclear Argonautes and/or H3K9 methyltransferases on both dosage compensation and global gene expression during somatic development. Our immunofluorescence and bioinformatic analyses suggest that the nuclear RNAi and H3K9me pathways are involved in the packaging of the X chromosomes during dosage compensation, without consequence to their transcriptional output. Instead, mutant RNAi mutants exhibit global transcriptional differences, in which HRDE-1 and NRDE-3 affect expression of their native targets through different modes of regulation and different relationships between each nuclear Argonaute and H3K9 methylation.
2024-10-01 | GSE277005 | GEO
Project description:Histone H3 Lys 4 methylation (H3K4me) is deposited by the conserved SET1/MLL methyltransferases acting in multiprotein complexes including Ash2 and Wdr5. While individual subunits contribute to complex activity, how they influence gene expression in a specific tissue remains largely unknown. In caenorhabditis elegans, SET-2/SET1, WDR-5.1 and ASH-2 are differentially required for germline H3K4 methylation. Using expression profiling on germlines from animals lacking set-2, ash-2 or wdr-5.1, we show that these subunits play unique and redundant functions to promote expression of germline genes and repress somatic genes. We further show that in set-2 and wdr-5.1 deficient germlines, somatic gene misexpression is associated with conversion of germ cells into somatic cells, and that nuclear RNAi acts in parallel with SET-2 and WDR-5.1 to maintain germline identity. These findings uncover a unique role for SET-2 and WDR-5.1 in preserving germline pluripotency, and underline the complexity of the cellular network regulating this process. Gene misregulation in SET1/set-2, wdr-5.1 and ash-2 defective germlines
2014-09-04 | E-GEOD-61094 | biostudies-arrayexpress
Project description:Histone H3 Lys 4 methylation (H3K4me) is deposited by the conserved SET1/MLL methyltransferases acting in multiprotein complexes including Ash2 and Wdr5. While individual subunits contribute to complex activity, how they influence gene expression in a specific tissue remains largely unknown. In caenorhabditis elegans, SET-2/SET1, WDR-5.1 and ASH-2 are differentially required for germline H3K4 methylation. Using expression profiling on germlines from animals lacking set-2, ash-2 or wdr-5.1, we show that these subunits play unique and redundant functions to promote expression of germline genes and repress somatic genes. We further show that in set-2 and wdr-5.1 deficient germlines, somatic gene misexpression is associated with conversion of germ cells into somatic cells, and that nuclear RNAi acts in parallel with SET-2 and WDR-5.1 to maintain germline identity. These findings uncover a unique role for SET-2 and WDR-5.1 in preserving germline pluripotency, and underline the complexity of the cellular network regulating this process.
2014-09-04 | GSE61094 | 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
Project description:Germline small RNA pathways initiate silencing of repetitive elements in animals and an interplay of nuclear small RNAs and chromatin modifications maintain this silencing, protecting the germline from spreading of transposable elements. In C. elegans germline, nuclear argonaute protein HRDE-1 initiates the transcriptional silencing pathway that is crucial for long term and heritable silencing of genes and repetitive regions. Here, we show that HRDE-1 interacts with components of the splicing machinery and the exon-junction complex. One such factor is the conserved RNA helicase EMB-4/AQR that binds introns and recruits the exon-junction proteins to newly spliced RNA. Our data shows that EMB-4/AQR is required for the transcriptional silencing pathway initiated by HRDE-1 and it functions by removing the intronic barriers to silencing thorugh its helicase function.
2017-06-30 | PXD004416 | Pride
Project description:Germline- and soma-specific heritable epigenetic silencing at an endogenous locus (RNA-Seq)
| PRJNA322338 | ENA
Project description:Epigenetic inheritance contributes fundamentally to transgenerational physiology and fitness. Mechanistic understanding of RNA-mediated chromatin modification and transgenerational epigenetic inheritance, which in C. elegans can be triggered by exogenous double-stranded RNA (exo-dsRNA) or facilitated by endogenous small interfering RNAs (endo-siRNAs), has mainly been limited to the post-initiation phases of silencing. Indeed, the dynamic process by which nuclear RNAi engages a transcriptionally active target, before the repressive state is stably established, remains largely a mystery. Here we found that the onset of exo-dsRNA-induced nuclear RNAi is a transgenerational process, and that establishment requires SET-32, one of the three putative histone methyltransferases (HMTs) that are required for H3K9me3 deposition at the nuclear RNAi targets. We also performed multigenerational whole-genome analyses to examine the establishment of silencing at endogenous targets of germline nuclear RNAi. The nuclear Argonaute (AGO) protein HRDE-1 is essential for the maintenance of nuclear RNAi. Repairing a loss-of-function mutation in hrde-1 by CRISPR restored the silencing of endogenous targets in animals carrying wild type set-32. However, for numerous endogenous targets, repairing the hrde-1 mutation in a set-32;hrde-1 double mutant failed to restore their silencing states in up to 20 generations after the hrde-1 repair, using a similar genome editing approach. We found that despite a prominent role in the establishment of silencing, however, set-32 is completely dispensable for the maintenance of silencing once HRDE-1-dependent gene repression is established. Our study indicates that: 1) initiation and maintenance of siRNA-guided transcriptional repression are two distinct processes with different genetic requirements; and 2) the rate-limiting step of the establishment phase is a transgenerational, chromatin-based process. In addition, our study reveals a novel paradigm in which a heterochromatin factor primarily functions to promote the initiation of transgenerational silencing, expanding mechanistic understanding of the well-recognized role of heterochromatin in epigenetic maintenance.
2018-07-26 | GSE117660 | GEO