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]
| PRJNA345015 | ENA
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: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: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: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: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.
2024-12-06 | GSE269096 | GEO
Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.
2023-05-26 | PXD028824 | Pride
Project description:The movement of repetitive elements in the germline creates widespread genomic alterations and pressure for resolution. Here we show that the Caenorhabditis clade took advantage of two transposon expansions by integrating hundreds of elements into its germline transcriptional network. We find that about one-third of C. elegans germline-specific promoters have been co-opted from CERP2 and CELE2 MITE elements and are regulated by HIM-17, a THAP domain-containing transcription factor related to a transposase. An ancestral CERP2 expansion took place in the common Caenorhabditis ancestor, concurrently with mutations in HIM-17 fixed by positive selection, whereas CELE2 expanded only in C. elegans. Through comparative analyses in C. briggsae, we find conservation as well as species-specific CERP2 co-option. Our work reveals the emergence of a novel transcriptional network driven by TE co-option and its impact on regulatory evolution.
2021-12-26 | GSE192539 | GEO
Project description:The movement of repetitive elements in the germline creates widespread genomic alterations and pressure for resolution. Here we show that the Caenorhabditis clade took advantage of two transposon expansions by integrating hundreds of elements into its germline transcriptional network. We find that about one-third of C. elegans germline-specific promoters have been co-opted from CERP2 and CELE2 MITE elements and are regulated by HIM-17, a THAP domain-containing transcription factor related to a transposase. An ancestral CERP2 expansion took place in the common Caenorhabditis ancestor, concurrently with mutations in HIM-17 fixed by positive selection, whereas CELE2 expanded only in C. elegans. Through comparative analyses in C. briggsae, we find conservation as well as species-specific CERP2 co-option. Our work reveals the emergence of a novel transcriptional network driven by TE co-option and its impact on regulatory evolution.
2021-12-26 | GSE192538 | GEO