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TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

ABSTRACT: The PIWI protein MIWI2 and its associated PIWI-interacting RNAs (piRNAs) instruct DNA methylation of young active transposable elements (TEs) in the male germline. Here we show that MIWI2 associates with TEX15 in foetal gonocytes. TEX15 is predominantly a nuclear protein that is not required for piRNA biogenesis but is essential for piRNA-directed TE de novo methylation and silencing. In summary, TEX15 is an essential executor of mammalian piRNA-directed DNA methylation.

ORGANISM(S): Mus musculus

PROVIDER: GSE150350 | GEO | 2020/06/17

REPOSITORIES: GEO

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TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

Project description:The PIWI protein MIWI2 and its associated PIWI-interacting RNAs (piRNAs) instruct DNA methylation of young active transposable elements (TEs) in the male germline. Here we show that MIWI2 associates with TEX15 in foetal gonocytes. TEX15 is predominantly a nuclear protein that is not required for piRNA biogenesis but is essential for piRNA-directed TE de novo methylation and silencing. In summary, TEX15 is an essential executor of mammalian piRNA-directed DNA methylation.

2020-06-18 | PXD019087 | Pride

TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

2020-06-17 | E-MTAB-9090 | biostudies-arrayexpress

SPOCD1 is a novel executor of piRNA-directed DNA methylation that links MIWI2 to the de novo DNA methylation machiner

Project description:In mammals, the acquisition of the germline from the soma provides the germline with an essential challenge, the necessity to erase and reset genomic methylation. In the male germline RNA-directed DNA methylation silences young active transposable elements (TEs). The PIWI protein MIWI2 (PIWIL4) and its associated PIWI-interacting RNAs (piRNAs) are proposed to tether MIWI2 to nascent TE transcripts and instruct DNA methylation. The mechanism by which MIWI2 directs de novo TE methylation is poorly understood but central to the immortality of the germline. Here, we define the interactome of MIWI2 in foetal gonocytes that are undergoing de novo genome methylation and identify a novel MIWI2-associated factor, SPOCD1, that is essential for young TE methylation and silencing. The loss of Spocd1 in mice results in male specific infertility and does not impact on piRNA biogenesis nor localization of MIWI2 to the nucleus. SPOCD1 is a nuclear protein and its expression is restricted to the period of de novo genome methylation. We found SPOCD1 co-purified in vivo with DNMT3L and DNMT3A, components of the de novo methylation machinery as well as constituents of the NURD and BAF chromatin remodelling complexes. We propose a model whereby tethering of MIWI2 to a nascent TE transcript recruits repressive chromatin remodelling activities and the de novo methylation apparatus through its association with SPOCD1. In summary, we have identified a novel and essential executor of mammalian piRNA-directed DNA methylation.

2020-06-22 | PXD016701 | Pride

SPOCD1 is a novel executor of piRNA-directed DNA methylation that links MIWI2 to the de novo DNA methylation machinery

2020-06-01 | E-MTAB-7997 | biostudies-arrayexpress

SPOCD1 is a novel executor of piRNA-directed DNA methylation that links MIWI2 to the de novo DNA methylation machinery

Project description:In mammals, the acquisition of the germline from the soma provides the germline with an essential challenge, the necessity to erase and reset genomic methylation. De novo genome methylation re-encodes the epigenome including transposable element (TE) silencing. In the male germline RNA-directed DNA methylation silences young active TEs. The PIWI protein MIWI2 (PIWIL4) and its associated PIWI-interacting RNA (piRNAs) act to tether MIWI2 to nascent TE transcripts and instruct DNA methylation of the active TE. The mechanism by which MIWI2 directs de novo TE methylation is poorly understood but central to the immortality of the germline. Here, we define the interactome of MIWI2 in fetal gonocytes that are undergoing de novo genome methylation and identify a novel MIWI2-associated factor SPOCD1 that is essential for TE silencing. The loss of Spocd1 in mice phenocopies that of Miwi2-deficient mice and does not impact on piRNA biogenesis nor localization of MIWI2 to the nucleus. SPOCD1 is a nuclear protein and its expression is restricted to the period of de novo genome methylation. We found SPOCD1 co-purified in vivo with constituents of several repressive chromatin remodelling complexes (NURD and BAF) as well as DNMT3L and DNMT3A, components of the de novo methylation machinery. We propose a model whereby tethering of MIWI2 to a nascent TE transcript recruits repressive chromatin remodelling activities and the de novo methylation apparatus through its association with SPOCD1. In summary, we have identified a novel and essential executor of mammalian piRNA-directed DNA methylation.

2020-06-17 | GSE131377 | GEO

TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

Project description:TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

| PRJEB38393 | ENA

TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

Project description:TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

| PRJNA631836 | ENA

Epigenetic control of transposable elements in the mouse male germ line by Tex15

Project description:The piRNA biogenesis was evaluated in the mouse testes lacking TEX15. Total small RNAs, MILI-, and MIWI2-associated small RNAs from control (Tex15+/-) and Tex15(-/-) knock-out testes were sequenced. Data analysis revealed that the abundance of miRNAs and piRNAs was comparable between control and Tex15 knock-out testes, suggesting that loss of TEX15 function does not impair piRNA biogenesis. However, the relative abundance of MILI- and MIWI2-bound sense piRNAs derived from transposable elements was increased.

2020-11-27 | GSE107832 | GEO

TEX15 silences transposable elements in male germ cells

Project description:This SuperSeries is composed of the SubSeries listed below. DNA methylation is a major silencing mechanism of transposable elements (TEs). Here we report that TEX15, a testis-specific protein, is required for TE silencing. TEX15 is both cytoplasmic and nuclear in embryonic germ cells and functions during genome-wide epigenetic reprogramming. Tex15 mutant exhibits DNA hypomethylation in TEs at a level similar to Mili but not Miwi2 mutant. As loss of Tex15 causes TE de-silencing without abolishing piRNA production, our results identify TEX15 as a new essential epigenetic regulator that appears to function independently or downstream of the piRNA biogenesis machineries to silence TEs by DNA methylation in male germ cells.

2020-05-18 | GSE140571 | GEO

C19ORF84 connects piRNA and DNA methylation machineries to defend the mammalian germline

Project description:In the male mouse germline, PIWI-interacting RNAs (piRNAs), bound by the PIWI protein MIWI2 (PIWIL4), guide DNA methylation of young active transposons through SPOCD1. However, the underlying mechanisms of SPOCD1-mediated piRNA-directed transposon methylation and whether this pathway functions to protect the human germline remains unknown. We identified loss-of-function variants in human SPOCD1 that cause defective transposon silencing and male infertility. Through the analysis of one of these pathogenic alleles, we discovered that the uncharacterised protein C19ORF84 interacts with SPOCD1. DNMT3C, the DNA methyltransferase responsible for transposon methylation, associates with SPOCD1 and C19ORF84 in foetal gonocytes. Furthermore, C19ORF84 is essential for piRNA-directed DNA methylation and male mouse fertility. Finally, C19ORF84 mediates the in vivo association of SPOCD1 with the de novo methylation machinery. In summary, we have discovered a conserved role for the human piRNA pathway in transposon silencing and C19ORF84, an uncharacterised protein essential for orchestrating piRNA-directed DNA methylation.

2024-02-14 | PXD047331 | Pride

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