More than 25 million years ago, a virus infected primates and left some genetic material behind. Many such viral genes were passed on to future generations and eventually some of them became a permanent feature of the human genome. About 8 per cent of human DNA is estimated to have come from viruses; many segments appear to be “junk,” but a number of them have been found to have important functions. Syncytin-1 is one such gene.
In viruses, syncytin-1 produced a protein that helped it stick to host cells and fuse with them so that they could replicate without getting noticed by the host’s immune system, explained stem cell biologist Harry Moore from the University of Sheffield in an email interview. Syncytin-1 has been a gene of interest ever since it was discovered in human placenta, the organ that appears during pregnancy and mediates nutrient uptake by the foetus from the mother. It appeared that this gene was crucial for the formation of placenta and its altered expression was linked with conditions of abnormal placentation.
Syncytin is known to be more abundant in the first trimester embryo than later stages, but Moore and Bikem Soygur from Akdeniz University, Turkey, wanted to narrow down further. “We were surprised it was present on embryos before implantation,” said Moore. This indicated that syncytin may be playing a role in another hallmark of early embryonic development, implantation. They duo presented the results of their investigation in a paper published on April 12 in Human Reproduction journal.
Stickiness matters
Implantation is the stage at which the 5-7 day old embryo fixes itself on the wall of the uterus. To probe into syncytin’s possible role in implantation, the scientists looked at pre-implantation embryos donated for research to identify which cells of the embryo first produce the protein. They found that most of the syncytin was on cells which stick the embryo to the womb at implantation, suggesting syncytin is important at this stage.
The mechanism by which syncytin-1 facilitates implantation is still not entirely clear, but Moore presented a likely explanation: “Most probably (it does this) by helping the embryo to first stick to and then squeeze between the cells of the lining of the womb.”
Before this evolutionary event, and in other mammals, there have been genes identified that function similar to syncytin to enable embryo implantation and a placentation, explained Moore. “But they evolved, new retroviral infections occurred and if this was better for the embryo the genes were retained and the previous genes then became dysfunctional,” he said, adding that if not for this viral infection of our ancestors and subsequent incorporation of syncytin-1, humans probably would not have evolved.
Possible applications
Understanding early embryonic development is required for refining current treatments of pregnancy-related issues. The scientists look forward to being able to develop blood tests based on their results to identify pregnancies that might be at risk and also develop appropriate therapies. But before this, more functional studies are needed. “It will be necessary to see if embryos from women who suffer with conditions such as recurrent miscarriage have unusual syncytin production,” said Moore, adding that efforts were also underway to find better ways to mimic embryo implantation such as in 3D cell cultures in order to study the process more closely.
Nandita Jayaraj is a freelance writer based in Bengaluru.