The histone demethylase KDM3 prevents auto-immune piRNAs production in Drosophila
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ABSTRACT:
PROVIDER: PRJNA839350 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19268660.fastq.gz | Fastqsanger.gz | |||
| SRR19268661.fastq.gz | Fastqsanger.gz | |||
| SRR19268662.fastq.gz | Fastqsanger.gz | |||
| SRR19268663.fastq.gz | Fastqsanger.gz | |||
| SRR19268664.fastq.gz | Fastqsanger.gz |
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Project description:In animals, genome integrity of the germ line is protected from transposable element (TE) activity by small, non-coding, dedicated RNAs acting as an immune system against TEs, and called PIWI-interacting RNAs (piRNAs) (Czech et al. 2018, Ozata et al. 2018). In Drosophila, the production of piRNAs is initiated from heterochromatic loci containing remnants of TEs and enriched in histone H3 trimethylated on lysine 9 (H3K9me3) (Brennecke et al. 2007, Gunarwardane et al. 2007; Rangan et al. 2011). These loci, called piRNA clusters, constitute a memory of past TE invasions. Little is known about how piRNA clusters are genetically defined. Using a genetic screen combined with a bimodal epigenetic state piRNA cluster (BX2), we identified the splicing factor Half pint (Hfp) and the histone demethylase KDM3 as being able to prevent BX2 piRNA production. Furthermore, we showed that Hfp is needed to splice Kdm3 transcripts. Germline expression of Kdm3 coding sequence (splicing-independent) rescued the hfp germline knock-down (GLKD) effect demonstrating that Kdm3 is sufficient to prevent BX2 piRNA production. Our data revealed that in the absence of Kdm3, dozens of gene-containing regions become bona fide germinal dual strand piRNA clusters. Indeed, they produce piRNAs originating from both DNA strands, become transcribed in a Moonshiner-dependent manner and enriched in di-and tri-methylation of lysine 9 of histone H3 (H3K9me2/3) and in Rhino, an HP1-like protein. Eggs laid by Kdm3 GLKD females do not hatch and show developmental defects phenocopying loss of function of genes included into the new piRNA clusters, suggesting an inheritance of functional ovarian “auto-immune” piRNAs. Our results demonstrate that some gene-containing regions are actively prevented for piRNA production by proteins that counteract piRNA cluster emergence. Hence, a non-piRNA-producing state is therefore not a "by default" state but rather a cellular lock that is actively controlled for some genomic loci.
2023-02-07 | GSE203279 | GEO
Project description:Genome integrity of the animal germline is protected from transposable element activity by PIWI-interacting RNAs (piRNAs). While piRNA biogenesis is intensively explored, little is known about the genetical determination of piRNA clusters, the genomic sources of piRNAs. Using a bimodal epigenetic state piRNA cluster (BX2), we identified the histone demethylase Kdm3 as being able to prevent a cryptic piRNA production. In the absence of Kdm3, dozens of coding gene-containing regions become genuine germline dual-strand piRNA clusters. Eggs laid by Kdm3 mutant females show developmental defects phenocopying loss of function of genes embedded into the additional piRNA clusters, suggesting an inheritance of functional ovarian "auto-immune" piRNAs. Antagonizing piRNA cluster determination through chromatin modifications appears crucial to prevent auto-immune genic piRNAs production.
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Project description:Production of artificial piRNAs in flies and mice
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Project description:In animals, a discrete class of small RNAs, the piwi-interacting RNAs (piRNAs), guard germ cell genomes against the activity of mobile genetic elements. piRNAs are generated, via an unknown mechanism, from apparently single-stranded precursors that arise from discrete genomic loci, termed piRNA clusters. The content of piRNA clusters, determines the capacity of the system to respond to a given element, in essence comprising an organism's evolving molecular definition of transposons. Presently, little is known about the signals that distinguish a locus as a source of piRNAs and about how abundant piRNAs are selected. To address these questions, we inserted new sequence information into piRNA clusters in mice and flies. In all cases, this information was incorporated into the piRNA repertoire and in one instance was shown to confer the ability to recognize and silence a corresponding element. Notably, patterns of piRNA abundance suggested that both intrinsic sequence and context with the cluster inform piRNA generation. Though piRNAs themselves are not conserved between species, the genomic location of clusters is often retained. We were able to create artificial piRNA clusters in non-native contexts in both mice and flies, indicating that the signals that define these as generative loci must lie within the clusters themselves rather than being implicit in their genomic position.
2012-01-01 | GSE32435 | GEO
Project description:In animals, a discrete class of small RNAs, the piwi-interacting RNAs (piRNAs), guard germ cell genomes against the activity of mobile genetic elements. piRNAs are generated, via an unknown mechanism, from apparently single-stranded precursors that arise from discrete genomic loci, termed piRNA clusters. The content of piRNA clusters, determines the capacity of the system to respond to a given element, in essence comprising an organism's evolving molecular definition of transposons. Presently, little is known about the signals that distinguish a locus as a source of piRNAs and about how abundant piRNAs are selected. To address these questions, we inserted new sequence information into piRNA clusters in mice and flies. In all cases, this information was incorporated into the piRNA repertoire and in one instance was shown to confer the ability to recognize and silence a corresponding element. Notably, patterns of piRNA abundance suggested that both intrinsic sequence and context with the cluster inform piRNA generation. Though piRNAs themselves are not conserved between species, the genomic location of clusters is often retained. We were able to create artificial piRNA clusters in non-native contexts in both mice and flies, indicating that the signals that define these as generative loci must lie within the clusters themselves rather than being implicit in their genomic position. Total RNA and RNA associated with Piwi proteins were isolated and size-fractionated by PAGE into 19-33nt. These were processed and sequenced on the Illumina GA2 platform.
2012-01-01 | E-GEOD-32435 | biostudies-arrayexpress
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Project description:We report that full length TET1 (TET1-FL) overexpression fails to induce global DNA demethylation in HEK293T cells. The preferential binding of TET1-FL to hypomethylated CpG islands (CGIs) through its CXXC domain leads to its inhibited 5-hydroxymethylcytosine (5hmC) production as methylation level increases. TET1-FL-induced 5hmC accumulates at CGI edges, while TET1 knockdown induces methylation spreading from methylated edges into hypomethylated CGIs. However, TET1 can regulate gene transcription independent of its dioxygenase catalytic function. Thus, our results identify TET1 as a maintenance DNA demethylase that does not purposely decrease methylation levels, but specifically maintains the DNA hypomethylation state of CGIs in adult cells. hMeDIP-seq analysis of genomic 5-hydroxymethylcytosine in HEK293T cells overexpressing mTET1-CD, TET1-CD, mTET1-FL, or TET1-FL
2014-06-04 | E-GEOD-44036 | biostudies-arrayexpress
Project description:We report that full length TET1 (TET1-FL) overexpression fails to induce global DNA demethylation in HEK293T cells. The preferential binding of TET1-FL to hypomethylated CpG islands (CGIs) through its CXXC domain leads to its inhibited 5-hydroxymethylcytosine (5hmC) production as methylation level increases. TET1-FL-induced 5hmC accumulates at CGI edges, while TET1 knockdown induces methylation spreading from methylated edges into hypomethylated CGIs. However, TET1 can regulate gene transcription independent of its dioxygenase catalytic function. Thus, our results identify TET1 as a maintenance DNA demethylase that does not purposely decrease methylation levels, but specifically maintains the DNA hypomethylation state of CGIs in adult cells. Genome-wdie profiling of gene expression in HEK293T cells following overexpression of wild type or catalytically mutant TET1-FL or TET1-CD
2014-06-04 | E-GEOD-49833 | biostudies-arrayexpress
Project description:Production of functional oocytes requires maternally expressed PIWI genes and piRNAs in golden hamsters
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Project description:The piRNA pathway controls transposon expression in animal germ cells, thereby ensuring genome stability over generations. piRNAs are maternally deposited and required for proper transposon silencing in adult offspring. However, a long-standing question in the field is the precise function of maternally deposited piRNAs and its associated factors during embryogenesis. Here, we probe the spatio-temporal expression patterns of several piRNA pathway components during early stages of development. Amongst those, factors required for transcriptional gene silencing (TGS) showed ubiquitous abundance in somatic and pole cells throughout the first half of embryogenesis. We further analysed the transcriptomes of various embryo stages and correlated these with the presence of selected chromatin marks. We found that a number of transposon families show bursts of transcription during early embryonic stages. Transposons heavily targeted by maternally deposited piRNAs accumulated repressive chromatin marks following their spike in expression. Furthermore, depletion of maternally deposited Piwi protein in early embryos resulted in increased expression of transposons targeted by inherited piRNAs and was accompanied by a strong loss of repressive chromatin marks at coding sequences. Overall, our data suggests a pivotal role for the piRNA pathway in transposon defence during Drosophila embryogenesis in somatic cells.
2021-07-26 | PXD022409 | Pride