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Piwi is required during Drosophila embryogenesis to license dual-strand piRNA clusters for transposon repression in adult ovaries [ChIP-seq]

ABSTRACT: Most piRNAs in the Drosophila female germline are transcribed from heterochromatic regions called dual-strand piRNA clusters. Histone 3 lysine 9 trimethylation (H3K9me3) is required for licensing piRNA production by these clusters. However, it is unclear when and how they acquire this permissive heterochromatic state. Although it has been suggested that piRNA cluster licensing is Piwi-independent, here we show that transient Piwi depletion in Drosophila embryos, using a refined knock-down system, results in H3K9me3 decrease at piRNA clusters. This is accompanied by aberrant maturation of piRNA precursor transcripts, accumulation of transposable element transcripts and female sterility. Conversely, Piwi knock-down at later developmental stages does not disturb piRNA cluster licensing, as previously reported. These results indicate that the identity of piRNA clusters is epigenetically acquired in a Piwi-dependent manner during a limited embryonic development window, which is reminiscent of the widespread genome reprogramming occurring during early mammalian zygotic development.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE83234 | GEO | 2017/04/27

SECONDARY ACCESSION(S): PRJNA325319

REPOSITORIES: GEO

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Piwi is required during Drosophila embryogenesis to license dual-strand piRNA clusters for transposon repression in adult ovaries [smallRNA-seq]

Project description:Most piRNAs in the Drosophila female germline are transcribed from heterochromatic regions called dual-strand piRNA clusters. Histone 3 lysine 9 trimethylation (H3K9me3) is required for licensing piRNA production by these clusters. However, it is unclear when and how they acquire this permissive heterochromatic state. Although it has been suggested that piRNA cluster licensing is Piwi-independent, here we show that transient Piwi depletion in Drosophila embryos, using a refined knock-down system, results in H3K9me3 decrease at piRNA clusters. This is accompanied by aberrant maturation of piRNA precursor transcripts, accumulation of transposable element transcripts and female sterility. Conversely, Piwi knock-down at later developmental stages does not disturb piRNA cluster licensing, as previously reported. These results indicate that the identity of piRNA clusters is epigenetically acquired in a Piwi-dependent manner during a limited embryonic development window, which is reminiscent of the widespread genome reprogramming occurring during early mammalian zygotic development.

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Piwi is required during Drosophila embryogenesis to license dual-strand piRNA clusters for transposon repression in adult ovaries [RNA-seq]

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The Rhino-Deadlock-Cutoff complex licenses non-canonical transcription of dual-strand piRNA clusters in Drosophila

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Trans-generationally inherited piRNAs trigger piRNA biogenesis by changing the chromatin of piRNA clusters and inducing precursor processing [cuff smallRNA]

Project description:Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. small RNA (19-29nt) sequencing of RNA from ovaries of cuff+/- or cuff-/- flies

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Project description:Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. nuclear run-on in wildtype and Rhino knockdown to investigate the transcriptional activity in Rhino knockdown compared to wildtype

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