Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).
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: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: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.
