RG motifs promote piRNA-mediated gene silencing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1260053 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33465510.fastq.gz | Fastqsanger.gz | |||
| SRR33465511.fastq.gz | Fastqsanger.gz | |||
| SRR33465512.fastq.gz | Fastqsanger.gz | |||
| SRR33465513.fastq.gz | Fastqsanger.gz | |||
| SRR33465514.fastq.gz | Fastqsanger.gz |
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Project description:PIWI-interacting RNAs (piRNAs) promote fertility in many animals. Yet, whether this is due to their conserved role in repressing repetitive elements (REs) or other functions remains unclear. Here, we show that the progressive loss of fertility in Caenorhabditis elegans lacking piRNAs is not caused by derepression of REs or other piRNA targets, but rather mediated by the epigenetic silencing of all the replicative histone genes. In the absence of piRNAs, downstream components of the piRNA pathway relocalize from germ granules and piRNA targets to histone mRNAs to synthesize antisense small RNAs (sRNAs) and induce transgenerational silencing. Removal of the downstream components of the piRNA pathway is sufficient to restore histone mRNA expression and fertility in piRNA mutants, and the inheritance of histone sRNAs in wild-type worms adversely affects their fertility for multiple generations. We conclude that the transgenerational silencing of histone genes contributes to the progressive loss of fertility in piRNA mutants and that coupling piRNAs and histone silencing may serve to maintain piRNAs production across evolution.
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Project description:The ability to distinguish non-self from self is the key characteristic for any defense system. piRNAs function as guardians of the genome by silencing non-self nucleic acids and transposable elements in animals. Many piRNA factors are enriched in perinuclear germ granules, but whether their localization is required for piRNA biogenesis or function is not known. Here we show that GLH/VASA helicase mutants exhibit defects in forming perinuclear condensates containing PIWI and other small RNA cofactors. These mutant animals produce largely normal levels of piRNA but are defective in triggering piRNA silencing. Strikingly, while many piRNA targets are activated in GLH mutants, we observed that hundreds of endogenous genes are aberrantly silenced by piRNAs. This defect in self versus non-self recognition was also observed in other mutants where perinuclear P granules are disrupted. Together, our results argue that perinuclear germ granules function critically to promote the fidelity of piRNA-based transcriptome surveillance in C. elegans and preserve self versus non-self distinction.
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Project description:Topoisomerase 3b Facilitates piRNA Biogenesis to Promote Transposon Silencing and Germ Cell Development
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Project description:PIWI-interacting RNAs (piRNAs) promote fertility in many animals. Yet, whether this is due to their conserved role in repressing repetitive elements (REs) remains unclear. Here, we show that the progressive loss of fertility in Caenorhabditis elegans lacking piRNAs is not caused by derepression of REs or other piRNA targets, but rather mediated by the epigenetic silencing of all the replicative histone genes. In the absence of piRNAs, downstream components of the piRNA pathway relocalize from germ granules and piRNA targets to histone mRNAs to synthesize antisense small RNAs (sRNAs) and induce transgenerational silencing. Removal of the downstream components of the piRNA pathway restores histone mRNA expression and fertility in piRNA mutants, and the inheritance of histone sRNAs in wild-type worms adversely affects their fertility for multiple generations. We conclude that the sRNA-mediated silencing of histone genes impairs fertility of piRNA mutants and may serve to maintain piRNAs across evolution.
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Project description:The PIWI-interacting RNA (piRNA) pathway is an important mechanism to suppress transposon activation in the germline that is highly conserved between Drosophila and mammals. This pathway starts from transcribing piRNA clusters to generate long piRNA precursors. The majority of piRNA clusters lacks a conventional promoter, and therefore their transcription is considered to utilize a noncanonical mechanism. However, information regarding transcriptional regulation of piRNA clusters is limited. Here, we report that the fly KAT6 acetyltransferase, Enok, is important for transposon silencing in the germline. Further small RNA-seq analysis revealed that Enok is critical for piRNA production from a specific subset of piRNA clusters including 42AB, one of the two major sources of piRNAs. Enok is the major enzyme for establishing the H3K23ac mark, and was shown to promote gene expression by acetylating H3K23. Surprisingly, our RNA-seq and ChIP-seq/ChIP-qPCR results suggest that Enok regulates expression of genes involved in the piRNA production by H3K23ac-dependent mechanisms, and also promotes transcription at piRNA clusters through H3K23ac-independent pathways. Our co-immunoprecipitation assay further suggests that Enok interacts with RNA polymerase II to facilitate transcription of piRNA clusters. Taken together, our study provides novel insights into the regulation of noncanonical transcription at piRNA clusters and transposon silencing.
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Project description:The PIWI-interacting RNA (piRNA) pathway is an important mechanism to suppress transposon activation in the germline that is highly conserved between Drosophila and mammals. This pathway starts from transcribing piRNA clusters to generate long piRNA precursors. The majority of piRNA clusters lacks a conventional promoter, and therefore their transcription is considered to utilize a noncanonical mechanism. However, information regarding transcriptional regulation of piRNA clusters is limited. Here, we report that the fly KAT6 acetyltransferase, Enok, is important for transposon silencing in the germline. Further small RNA-seq analysis revealed that Enok is critical for piRNA production from a specific subset of piRNA clusters including 42AB, one of the two major sources of piRNAs. Enok is the major enzyme for establishing the H3K23ac mark, and was shown to promote gene expression by acetylating H3K23. Surprisingly, our RNA-seq and ChIP-seq/ChIP-qPCR results suggest that Enok regulates expression of genes involved in the piRNA production by H3K23ac-dependent mechanisms, and also promotes transcription at piRNA clusters through H3K23ac-independent pathways. Our co-immunoprecipitation assay further suggests that Enok interacts with RNA polymerase II to facilitate transcription of piRNA clusters. Taken together, our study provides novel insights into the regulation of noncanonical transcription at piRNA clusters and transposon silencing.
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Project description:The PIWI-interacting RNA (piRNA) pathway is an important mechanism to suppress transposon activation in the germline that is highly conserved between Drosophila and mammals. This pathway starts from transcribing piRNA clusters to generate long piRNA precursors. The majority of piRNA clusters lacks a conventional promoter, and therefore their transcription is considered to utilize a noncanonical mechanism. However, information regarding transcriptional regulation of piRNA clusters is limited. Here, we report that the fly KAT6 acetyltransferase, Enok, is important for transposon silencing in the germline. Further small RNA-seq analysis revealed that Enok is critical for piRNA production from a specific subset of piRNA clusters including 42AB, one of the two major sources of piRNAs. Enok is the major enzyme for establishing the H3K23ac mark, and was shown to promote gene expression by acetylating H3K23. Surprisingly, our RNA-seq and ChIP-seq/ChIP-qPCR results suggest that Enok regulates expression of genes involved in the piRNA production by H3K23ac-dependent mechanisms, and also promotes transcription at piRNA clusters through H3K23ac-independent pathways. Our co-immunoprecipitation assay further suggests that Enok interacts with RNA polymerase II to facilitate transcription of piRNA clusters. Taken together, our study provides novel insights into the regulation of noncanonical transcription at piRNA clusters and transposon silencing.
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Project description:PIWI-interacting RNAs (piRNAs) promote fertility in many animals. Yet, whether this is due to their conserved role in repressing repetitive elements (REs) remains unclear. Here, we show that the progressive loss of fertility in Caenorhabditis elegans lacking piRNAs is not caused by derepression of REs or other piRNA targets, but rather mediated by the epigenetic silencing of all the replicative histone genes. In the absence of piRNAs, downstream components of the piRNA pathway relocalize from germ granules and piRNA targets to histone mRNAs to synthesize antisense small RNAs (sRNAs) and induce transgenerational silencing. Removal of the downstream components of the piRNA pathway restores histone mRNA expression and fertility in piRNA mutants, and the inheritance of histone sRNAs in wild-type worms adversely affects their fertility for multiple generations. We conclude that the sRNA-mediated silencing of histone genes impairs fertility of piRNA mutants and may serve to maintain piRNAs across evolution.
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