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.
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.
Project description:We repport the effect of Tex15 inactivation on the transcriptome of male germ cells at embryonic day 16.5 (e16.5), 18.5 (e18.5), and postnatal day 2 (d2). We find upregulation of a large number of transposable elements in Tex15-/- germ cells.
Project description: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. Through WGBS, we find that Tex15 mutant germ cells exhibit DNA hypomethylation in TEs. 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.
Project description: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 expressed in embryonic germ cells and functions during genome-wide epigenetic reprogramming. The Tex15 mutant exhibits DNA hypomethylation in TEs at a level similar to Mili and Dnmt3c but not Miwi2 mutants. TEX15 is associated with MILI in testis. As loss of Tex15 causes TE desilencing with intact piRNA production, our results identify TEX15 as a new essential epigenetic regulator that may function as a nuclear effector of MILI to silence TEs by DNA methylation.
Project description:We repport the effect of Tex15 inactivation on the transcriptome of male germ cells at embryonic day 16.5 (e16.5), 18.5 (e18.5), and postnatal day 2 (d2). We find a large number of differentially expressed genes between Tex15-deficient and Tex15 heterozygous germ cells at e18.5 and d2 but much fewer differentially expressed genes at e16.5.
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.