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

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 hypom...

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Detalles Bibliográficos
Autores principales: Yang, Fang, Lan, Yemin, Pandey, Radha Raman, Homolka, David, Berger, Shelley L., Pillai, Ramesh S., Bartolomei, Marisa S., Wang, P. Jeremy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2020
Materias:
Research Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263141/
https://www.ncbi.nlm.nih.gov/pubmed/32381626
http://dx.doi.org/10.1101/gad.335489.119
Descripción
Sumario: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.

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