The activity and structure of transposable elements (TEs) have a profound impact on architecture and function of host genome. Over evolutionary time, TEs are responsible for beneficial genetic innovations in the host system. However, in the short term, TE-induced events can lead to various difficulties, such as congenital disease, infertility and cancer. Thus, the host has evolved silencing pathways to minimize TE activity; DNA methylation, repressive histone marks and RNAi.
This paper focuses on epigenetic mechanisms for TE silencing during meiosis in mouse, and demonstrates that DNA methylation restrains particular TEs from adopting chromatin characteristics amenable to meiotic recombination.