Figure 1.

Endogenous retroviral elements (ERVs) result from the occasional infection of a germline cell by a retrovirus, whose (potentially) defective offspring is transmitted further as a provirus in a Mendelian fashion. ERVs typically encode the canonical retroviral proteins GAG (group-specific antigens; capsid and matrix protein), POL (RT, reverse transcriptase; IN, integrase), and ENV (envelope). The ERVs are divided into three classes based on the sequence conservation with active retrovirus; class I (eMLVs), class II (musD/ETn/IAPs), and class III (ERV-L). ERVs are flanked by LTRs (green boxes) of 300–1,200 nucleotides as a result of the retrotransposition event. Class III ERVs make up almost 5% of the mouse genome and consists of muERV-L/MERVL elements (depicted) and the non-autonomous mammalian apparent LTR retrotransposons (MaLRs). The muERV-L family members have Gag and Pol genes but no detectable Env, a dUTPase gene (not shown). For the lack of ENV they are defective for cell to cell transmission. In addition to muERV-L, the mouse genome contains many thousands of ERV-L derived LTR elements termed MT2-Mm. LTRs are bound by transcription factors (TF) that drive transcription. ERV elements may also bind TF in the body of their genes, probably influencing chromatin dynamics or surveillance. After initial insertion (and transposition), ERVs over time may accumulate mutations and have contributed significantly to the generation of new transcription factor binding sites and hence impact on gene expression, genome function, and evolution. Transposon-derived promoters drive expression of alternative transcripts, including many of the LncRNAs detected by the ENCODE project, orchestrate stage, and tissue-dependent transcription, or serve as alternate promoters.