Turnover of syncytiotrophoblast in a human placental villus
Syncytiotrophoblast lacks inner cell boundaries but contains multiple nuclei. One place where it occurs is the surface of human placental villi. Syncytiotrophoblast has a high turnover rate and is continually replenished from the cytotrophoblast. This requires fusion of cytotrophoblasts with the existing syncytiotrophoblast, a process promoted by syncytins.
Syncytins are genes of retroviral origin that have been incorporated into the genome and are expressed in the placenta where they promote cell fusion to form the multinucleated syncytiotrophoblast. As recently reviewed in Placenta, syncytins have been discovered in primates, muroid rodents (such as the mouse), rabbits and carnivores. The search continues.
A retrovirus is an RNA virus that replicates in a host cell. It uses reverse transcriptase to produce DNA from its own RNA genome. The DNA is then incorporated into the genome of the host cell. This DNA can be transcribed to RNA and translated to viral proteins. Perhaps the best known example is human immunodeficiency virus 1 (HIV-1). Most retroviruses infect somatic cells, but occasionally infection of germ line cells occurs, resulting in creation of an endogenous retrovirus (ERV). The genome of mammals is littered with ERVs. Most have been inactivated in the course of evolution. A few, however, are not only expressed but show evidence of purifying selection.
The envelope (env) genes of retroviruses function to promote fusion of the viral membrane with the plasma membrane of a host cell. Syncytins are derived from env genes and are expressed in the placenta, where they promote fusion of cytotrophoblasts with the syncytiotrophoblast. Thus far six syncytin genes have been discovered including two in the mouse and two in higher primates. These genes are not orthologous so each represents an independent capture from a retrovirus. Yet another example of convergent evolution!
There is more. The envelope protein of retroviruses is immunosuppressive and endogenous env genes may contribute to immune tolerance by the mother of the fetal semi-allograft.