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The mouse genome is replete with retrotransposon sequences, from evolutionarily young elements with mutagenic potential that must be controlled, to inactive molecular fossils whose sequences can be domesticated over evolutionary time to benefit the host genome. In an exciting new study, de la Rica and colleagues have uncovered a complex relationship between ten-eleven translocation (TET) proteins and retrotransposons in mouse embryonic stem cells (ESCs), implicating TETs as enhancers in the exaptation and function of retroelement sequences. Furthermore, they have demonstrated that active demethylation of retrotransposons does not correlate with their increased expression in ESCs, calling into question long-held assumptions regarding the importance of DNA demethylation for retrotransposon expression, and revealing novel epigenetic players in retrotransposon control. Please see related Research article:http://genomebiology.biomedcentral.com/articles/10.1186/s13059-016-1096-8
Gerdes, P., Richardson, S. R., & Faulkner, G. J. (2016). TET enzymes: Double agents in the transposable element-host genome conflict. Genome Biology, 17(1). https://doi.org/10.1186/s13059-016-1124-8