Abstract
The ongoing activity of the human retrotransposon Long Interspersed Element 1 (LINE-1 or L1) continues to impact the human genome in various ways. Throughout evolution, mammalian and primate genomes have been under selection to generate strategies to reduce the activity of selfish DNA like L1. Similarly, selfish DNA has evolved to elude these containment systems. This intragenomic conflict has left many inactive versions of LINEs and other Transposable Elements (TEs) littering the human genome, which together account for roughly half of our DNA. Here, we survey the distinct mechanisms operating in the human genome that seem to reduce the mobility of L1s. In addition, we discuss recent findings that strongly suggest epigenetic mechanisms specifically regulate L1 activity in pluripotent human cells.