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Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus

ABSTRACT: Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus

PROVIDER: PRJNA937771 | ENA |

REPOSITORIES: ENA

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Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [RNA-Seq]

Project description:Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [RNA-Seq]

| PRJNA937769 | ENA

Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [ATAC-Seq]

Project description:Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [ATAC-Seq]

| PRJNA1005682 | ENA

Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [small RNA-Seq]

Project description:Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [small RNA-Seq]

| PRJNA937774 | ENA

Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [ATAC-Seq]

Project description:The PIWI-interacting RNA (piRNA) pathway plays a crucial role in preventing endogenous genomic parasites, transposable elements (TEs), from damaging the genetic material of animal gonadal cells. Specific regions in the genome, called piRNA clusters, define each species’ piRNA repertoire and therefore its capacity to recognize and silence transposons. In the somatic cells of the Drosophila melanogaster ovary, the flamenco (flam) unistrand cluster is the main source of piRNAs and primarily regulates Gypsy family TEs that are able to form virus-like particles and infect neighbouring germ cells. Disruption of the flam locus or failure to process flam precursor transcripts into piRNAs results in sterility, yet it remains unknown whether this silencing mechanism is employed widely across Drosophilidae. Here, using both synteny-based analyses and de novo TE annotation, we identify candidate loci sharing both their organisation and TE targeting repertoire with flam in widely divergent Drosophila species groups. Small RNA-sequencing validated these loci as bona-fide unistrand piRNA clusters and revealed their predominant expression in somatic cells of the ovary, likely to counter TE mobilisation in this tissue. This study provides compelling evidence of co-evolution between virus-like Gypsy family transposons and a host defence mechanism in form of soma-expressed, unistrand piRNA clusters.

2023-09-26 | GSE240910 | GEO

Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [RNA-Seq]

2023-09-26 | GSE225887 | GEO

Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus [small RNA-Seq]

2023-09-26 | GSE225888 | GEO

Unistrand piRNA clusters are an evolutionarily conserved mechanism to suppress endogenous retroviruses across the Drosophila genus

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-26 | GSE225889 | GEO

Large Drosophila Germline piRNA Clusters are Evolutionarily Labile and Dispensable for Transposon Regulation

Project description:PIWI proteins and their guiding Piwi-interacting small RNAs (piRNAs) are crucial for fertility and transposon defense in the animal germline. In most species, the majority of piRNAs are produced from distinct large genomic loci, called piRNA clusters. It is assumed that germline-expressed piRNA clusters, particularly in Drosophila, act as master regulators to control the activity of transposons dispersed across the genome. Here, using synteny analysis, we show that large germline clusters are evolutionarily labile, arise at loci characterized by recurrent chromosomal rearrangements, and are mostly species-specific across the Drosophila genus. By engineering chromosomal deletions in D. melanogaster, we demonstrate that the three largest germline clusters, which the generation of >40% of all transposon-targeting piRNAs depend on, are neither required for fertility nor for the regulation of transposon activity in trans. We provide further evidence that dispersed active elements, rather than the regulatory action of large Drosophila germline clusters in trans, may be central for transposon defense.

2021-05-31 | GSE174561 | GEO

Large Drosophila Germline piRNA Clusters are Evolutionarily Labile and Dispensable for Transposon Regulation

Project description:Large Drosophila Germline piRNA Clusters are Evolutionarily Labile and Dispensable for Transposon Regulation

| PRJNA730546 | ENA

Acetyltransferase Enok regulates transposon silencing by promoting transcription at piRNA clusters and genes involved in piRNA biosynthesis [ncRNA-seq]

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.

2021-01-07 | GSE105099 | GEO

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