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

Genes Dev. 2020 Jun 1;34(11-12):745-750. doi: 10.1101/gad.335489.119. Epub 2020 May 7.


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.

Keywords: DNA methylation; MILI; TEX15; epigenetics; spermatogenesis; transposable element.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism*
  • DNA Methylation
  • DNA Transposable Elements / genetics*
  • Embryonic Germ Cells / metabolism
  • Epigenesis, Genetic
  • Gene Expression Regulation, Developmental / genetics
  • Gene Silencing / physiology*
  • Germ Cells / metabolism*
  • Male
  • Mice
  • Mutation


  • Cell Cycle Proteins
  • DNA Transposable Elements
  • Tex15 protein, mouse