Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA345014 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4319300.fastq.gz | Fastqsanger.gz | |||
| SRR4319310.fastq.gz | Fastqsanger.gz | |||
| SRR4319301.fastq.gz | Fastqsanger.gz | |||
| SRR4319311.fastq.gz | Fastqsanger.gz | |||
| SRR4319302.fastq.gz | Fastqsanger.gz |
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Project description:A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress [ChIP-seq]
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Project description:A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress
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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:The assembly of repressive heterochromatin domains in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA-based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeat elements are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) PhpCNF-Y complex, which includes histone fold domain proteins, can infiltrate constitutive heterochromatin to transcribe repeat elements. PhpCNF-Y collaborates with a Zn-finger containing TF to bind heterochromatic repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, PhpCNF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain cryptic introns that are processed via a mechanism requiring the spliceosome to generate small interfering RNAs (siRNAs) by the RNAi machinery. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for nucleation of heterochromatin at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.
2024-06-21 | MSV000095108 | MassIVE
Project description:The assembly of repressive heterochromatin in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA- based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeats are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) Php|NF-Y complex, which includes histone fold domain proteins, can infiltrate constitutive heterochromatin to transcribe repeat elements. Php|NF-Y collaborates with a Zn-finger containing TF to bind repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, Php|NF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain cryptic introns that are processed via a mechanism requiring the spliceosome to generate small interfering RNAs (siRNAs) by the RNAi machinery. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for heterochromatin nucleation at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.
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Project description:Repetitive sequences derived from transposons make up a large fraction of eukaryotic genomes and must be silenced to protect genome integrity. Repetitive elements are often found in heterochromatin; however, the roles and interactions of heterochromatin proteins in repeat regulation are poorly understood. Here we show that a diverse set of C. elegans heterochromatin proteins act together with the piRNA and nuclear RNAi pathways to silence repetitive elements and prevent genotoxic stress in the germ line. Mutants in genes encoding HPL-2/HP1, LIN-13, LIN-61, LET-418/Mi-2, and H3K9me2 histone methyltransferase MET-2/SETDB1 also show functionally redundant sterility, increased germline apoptosis, DNA repair defects, and interactions with small RNA pathways. Remarkably, fertility of heterochromatin mutants could be partially restored by inhibiting cep-1/p53, endogenous meiotic double strand breaks, or the expression of MIRAGE1 DNA transposons. Functional redundancy among these factors and pathways underlies the importance of safeguarding the genome through multiple means.
2017-03-11 | GSE87523 | GEO
Project description:Repetitive sequences derived from transposons make up a large fraction of eukaryotic genomes and must be silenced to protect genome integrity. Repetitive elements are often found in heterochromatin; however, the roles and interactions of heterochromatin proteins in repeat regulation are poorly understood. Here we show that a diverse set of C. elegans heterochromatin proteins act together with the piRNA and nuclear RNAi pathways to silence repetitive elements and prevent genotoxic stress in the germ line. Mutants in genes encoding HPL-2/HP1, LIN-13, LIN-61, LET-418/Mi-2, and H3K9me2 histone methyltransferase MET-2/SETDB1 also show functionally redundant sterility, increased germline apoptosis, DNA repair defects, and interactions with small RNA pathways. Remarkably, fertility of heterochromatin mutants could be partially restored by inhibiting cep-1/p53, endogenous meiotic double strand breaks, or the expression of MIRAGE1 DNA transposons. Functional redundancy among these factors and pathways underlies the importance of safeguarding the genome through multiple means.
2017-03-11 | GSE87522 | GEO
Project description:Regulation of germline gene expression in C. elegans germline stem cells.
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Project description:Histone H3K9 trimethylation (H3K9me3) plays a pivotal role in the establishment and maintenance of heterochromatin and is essential for facilitating epigenetic inheritance. H3K9me3 is often biasedly deposited and associated with repetitive sequence region, although the underlying mechanism remain poorly understood. In this study, we identify two proteins, SECP-1 and SECP-2, as crucial cofactors for the genome-wide deposition of H3K9me3 in Caenorhabditis elegans. SECP-1 interacts directly with SECP-2 and the primary H3K9me3 methyltransferase, SET-25, forming a protein complex that bridges SECP-2 with SET-25. This complex assembles in the cytoplasm and is transported into the nucleus through SET-25. Once in the nucleus, the complex is recruited to and concentrated at SET-25’s genomic targets in an interdependent manner. The accumulation of this complex correlates with the formation of condensates at repetitive sequences, the perinuclear localization of heterochromatin, and the epigenetic inheritance of small RNA-mediated gene silencing. The introduction of transgenic arrays leads to the redistribution of the SECP-1/SECP-2/SET-25 complex to the transgene locus, a genome-wide decrease in H3K9me3 levels, and an increase in repetitive sequence expression. We propose that repetitive sequences drive the formation of condensates containing H3K9me3 methyltransferase complexes, which in turn causes a biased deposition of H3K9me3 at these genomic regions.
2025-05-28 | GSE297991 | GEO
Project description:Histone H3K9 trimethylation (H3K9me3) plays a pivotal role in the establishment and maintenance of heterochromatin and is essential for facilitating epigenetic inheritance. H3K9me3 is often biasedly deposited and associated with repetitive sequence region, although the underlying mechanism remain poorly understood. In this study, we identify two proteins, SECP-1 and SECP-2, as crucial cofactors for the genome-wide deposition of H3K9me3 in Caenorhabditis elegans. SECP-1 interacts directly with SECP-2 and the primary H3K9me3 methyltransferase, SET-25, forming a protein complex that bridges SECP-2 with SET-25. This complex assembles in the cytoplasm and is transported into the nucleus through SET-25. Once in the nucleus, the complex is recruited to and concentrated at SET-25’s genomic targets in an interdependent manner. The accumulation of this complex correlates with the formation of condensates at repetitive sequences, the perinuclear localization of heterochromatin, and the epigenetic inheritance of small RNA-mediated gene silencing. The introduction of transgenic arrays leads to the redistribution of the SECP-1/SECP-2/SET-25 complex to the transgene locus, a genome-wide decrease in H3K9me3 levels, and an increase in repetitive sequence expression. We propose that repetitive sequences drive the formation of condensates containing H3K9me3 methyltransferase complexes, which in turn causes a biased deposition of H3K9me3 at these genomic regions.
2025-05-28 | GSE297992 | GEO