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 mutant exhibits DNA hypomethylation in TEs at a level similar to and but not mutants. TEX15 is associated with MILI in testis. As loss of 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.
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| http://dx.doi.org/10.1101/gad.335489.119 | DOI Listing |
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