The opitz syndrome gene mid1 is transcribed from a human endogenous retroviral promoter.
Human endogenous retroviruses (HERVs) and other long terminal repeat (LTR)–containing elements comprise a significant portion (8%) of the human genome and are likely vestiges of retroviral infections during primate evolution. Many of the HERVs present in human DNA have retained functional promoter, enhancer, and polyadenylation signals, and these regulatory sequences have the potential to modify t
