Dynamicdosage compensation of transposable elementsin mammals

In mammals, X-linked dosage compensation involves two processes: X-inactivation to balance X chromosome dosage between males and females, and X-hyperactivation to achieve X-autosome balance. Transposable elements (TEs) are repetitive mobile DNA sequences and major sources of X chromosome dosage. Current studies in X-linked dosage compensation mainly focus on genes, with TEs still remaining elusive. Here we use “So-Smart-Seq” to comprehensively determine the allelic dynamics of TEs in the context of imprinted and random X-chromosome inactivation (XCI). We find that chromosomal loci and genetic backgrounds significantly impact TE silencing, and reveal putative roles of SINEs in shaping 3D chromatin architectures. We show remarkable difference in TE silencing between two forms of XCI and discover that X-hyperactivation is absent in TEs. Our data provide deep insight for TE studies and greatly contribute to complete understanding of X-chromosome wide dosage compensation.