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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.

TEX15 associates with MILI and silences transposable elements in male germ cells