Genomic vagabonds: endogenous retroviruses and placental evolution.

Endogenous retroviruses (ERVs) appear to have a particular predilection for placentas: retroviral genes have repeatedly been coopted for placental functions. In this issue, Chuong draws attention to the important contribution of retroviral promoters in rewiring placental development [1]. He proposes that trophoblast cells provide a permissive epigenetic environment for ERV activity because placental development has become “addicted” to transcription from ERV-derived promoters. In this view, adaptations to shut down ERVs in trophoblast cells are unable to evolve because they would also inactivate key developmental pathways that use retroviral-LTRs as promoters. In a process of positive feedback, past cooption of LTRs favors continued ERV activity that predisposes to new cooption of LTRs and reinforcement of the addiction. This recursive process could help to explain the extraordinary diversity of placental structures among eutherian mammals. By definition, ERVs are inserted into germline DNA and inherited by every cell of the body. They can be transmitted vertically by replication with host DNA