Genetic polymorphisms lead to major, locus-specific, variation in piRNA production in mouse.
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ABSTRACT:
PROVIDER: PRJNA888107 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21838900.fastq.gz | Fastqsanger.gz | |||
| SRR21838901.fastq.gz | Fastqsanger.gz | |||
| SRR21838902.fastq.gz | Fastqsanger.gz | |||
| SRR21838903.fastq.gz | Fastqsanger.gz | |||
| SRR21838904.fastq.gz | Fastqsanger.gz |
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Project description:PIWI-interacting RNAs (piRNAs) are small noncoding RNAs that silence transposons in the animal germline. PiRNAs are produced from long single-stranded noncoding transcripts, from protein-coding transcripts, as well as from transposons. While some sites that produce piRNAs are in deeply conserved syntenic regions, in general, piRNAs and piRNA-producing loci turnover faster than other functional parts of the genome. To learn about the sequence changes that contribute to the fast evolution of piRNAs, we set out to analyze piRNA expression between genetically different mice. Here we report the sequencing and analysis of small RNAs from the mouse male germline of four classical inbred strains, one inbred wild-derived strain and one outbred strain. We find that genetic differences between individuals underlie variation in piRNA expression. We report significant differences in piRNA production at loci with endogenous retrovirus insertions. Strain-specific piRNA-producing loci include protein-coding genes. Our findings provide evidence that transposable elements contribute to inter-individual differences in expression, and potentially to the fast evolution of piRNA-producing loci in mammals.
2023-09-22 | GSE215030 | GEO
Project description:In the Drosophila germline, transposable elements (TEs) are silenced by PIWI-interacting RNA (piRNA) that originate from distinct genomic regions termed piRNA clusters and are processed by PIWI-subfamily Argonaute proteins. Here, we explore the variation in the ability to restrain an alien TE in different Drosophila strains. The I-element is a retrotransposon involved in the phenomenon of I-R hybrid dysgenesis in Drosophila melanogaster. Genomes of R strains do not contain active I-elements, but harbour remnants of ancestral I-related elements. The permissivity to I-element activity of R females, called reactivity, varies considerably in natural R populations, indicating the existence of a strong natural polymorphism in defense systems targeting transposons. To reveal the nature of such polymorphisms, we compared ovarian small RNAs between R strains with low and high reactivity and show that reactivity negatively correlates with the ancestral I-element-specific piRNA content. Analysis of piRNA clusters containing remnants of I-elements shows increased expression of the piRNA precursors and enrichment by the Heterochromatin Protein 1 homolog, Rhino, in weak R strains, which is in accordance with stronger piRNA expression by these regions. To explore the nature of the differences in piRNA production, we focused on two R strains, weak and strong, and showed that the efficiency of maternal inheritance of piRNAs as well as the I-element copy number are very similar in both strains. At the same time, germline and somatic uni-strand piRNA clusters generate more piRNAs in strains with low reactivity, suggesting the relationship between the efficiency of primary piRNA production and variable response to TE invasions. The strength of adaptive genome defense is likely driven by naturally occurring polymorphisms in the rapidly evolving piRNA pathway proteins. We hypothesize that hyper-efficient piRNA production is contributing to elimination of a telomeric retrotransposon HeT-A, which we have observed in one particular transposon-resistant R strain.
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Project description:In animal gonads, 23-30nt long PIWI interacting RNAs (piRNAs) guarantee genome integrity by guiding the sequence specific silencing of selfish genetic elements such as transposons. Two major branches of piRNA biogenesis, namely primary processing and ping-pong amplification, feed into the PIWI clade of Argonaute proteins. Despite our conceptual understanding of piRNA biogenesis, major gaps exist in the mechanistic understanding of the underlying molecular processes as well as in the knowledge of the involved players. Here, we demonstrate an essential role for the female sterility gene shutdown in the piRNA pathway. Shutdown, an evolutionarily conserved co-chaperone of the immunophilin class is the first piRNA biogenesis factor that is essential for all primary and secondary piRNA populations in Drosophila. Based on these findings, we define distinct groups of piRNA biogenesis factors and reveal the core concept of how PIWI family proteins are hard-wired into piRNA biogenesis processes.
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Project description:In animal gonads, 23-30nt long PIWI interacting RNAs (piRNAs) guarantee genome integrity by guiding the sequence specific silencing of selfish genetic elements such as transposons. Two major branches of piRNA biogenesis, namely primary processing and ping-pong amplification, feed into the PIWI clade of Argonaute proteins. Despite our conceptual understanding of piRNA biogenesis, major gaps exist in the mechanistic understanding of the underlying molecular processes as well as in the knowledge of the involved players. Here, we demonstrate an essential role for the female sterility gene shutdown in the piRNA pathway. Shutdown, an evolutionarily conserved co-chaperone of the immunophilin class is the first piRNA biogenesis factor that is essential for all primary and secondary piRNA populations in Drosophila. Based on these findings, we define distinct groups of piRNA biogenesis factors and reveal the core concept of how PIWI family proteins are hard-wired into piRNA biogenesis processes. small-RNA libraries from 2 control samples and 7 knock-down samples of D. mel. ovaries and 2 small-RNA profiles from Piwi IP and Aub IP from OSCs.
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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: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:Abstract: Akin to an adaptive immune system, PIWI-interacting small RNAs (piRNAs) protect the integrity of germline genomes by silencing mobile genetic elements. Precision of piRNA silencing is crucial, as failing to silence a single active transposon or wrongly silencing an essential gene threaten the survival of the species. How piRNAs discriminate between self and nonself and adapt during evolution remains a central question in reproductive biology. Target specificity is determined by basepairing complementarity and places the sequence of piRNAs at the heart of piRNA-guided self/nonself discrimination. Here, we characterize millions of piRNA sequences in flies and mice in search for conserved patterns that determine the specificity of piRNA-guided silencing. We identify two groups of piRNA sequences that differ in abundance, complexity and function. The first group represents the top 1% most abundant sequences and drives piRNA-silencing in a reporter assay. In contrast, the second group of sequences does not function in every cell, every individual or every generation. These rare piRNAs establishes cell-to-cell polymorphism and present opportunity for adaptation to novel genomic invaders during evolution. A model emerges that entrust a selected group of piRNA sequences to establish self/nonself discrimination for future generations, and another group to cultivate polymorphisms.
2021-07-30 | GSE156058 | GEO