Did ancient viruses spur human evolution

Viruses may be deadly, but the continual struggle has bound us together. Our DNA is not only a blueprint for our bodies, it is a living history of millions of years of conflict. Register or Log In. The Magazine Shop. Login Register Stay Curious Subscribe. Planet Earth. Newsletter Sign up for our email newsletter for the latest science news.

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By the s, however, enough genetic evidence had accumulated to show that Margulis was right. Symbiosis was responsible for some of the most significant evolutionary leaps in the history of the planet. Margulis, though, saw symbiosis everywhere and believed that this softer, gentler side of evolution was getting short shrift in research. Although most symbiosis research has focused on the role of the microbiome, the viruses tucked into our DNA can play a similar role in splitting apart two populations, turning one species into two.

The first wedge scientists discovered was a protein called syncytin. Boston in the mids was humming with the activity of the Human Genome Project. Sequencing technologies had advanced to the point where scientists were incorporating gene discovery into even the most basic research. Since the American courts had thus far allowed companies to patent the genes they discovered, companies like the Genetics Institute now a part of Pfizer saw a chance to cash in.

There, molecular biologist John McCoy was looking for proteins secreted by cells since they seemed good targets for developing potential drugs.

Before McCoy could go public with his discovery, he needed to figure out exactly what syncytin did, a job he passed to bench scientist Sha Mi, who everyone called Misha. Syncytin is produced only by certain cells in the placenta, and it directs the formation of the cellular boundary between the placenta and maternal tissue.

Approximately one week after fertilization, the egg, now a hollow ball of cells called a blastocyst, implants itself into the uterus, stimulating the formation of the placenta, which provides the fetus with oxygen and nutrients while removing carbon dioxide and other wastes.

It also serves as a barrier to prevent infection and keep maternal and fetal blood separate. Mixing the two could cause a fatal autoimmune response. The cells in the outer layer of the blastocyst form the outer layer of the placenta, and those in direct contact with the uterus are the only ones that made syncytin. When the scientists looked closer at the DNA sequence of syncytin, they found that it was nearly identical to a viral protein called env that caused the virus to fuse with its host cell.

In the placenta, syncytin performed helped the fetus fuse with its mother. At last McCoy, Howe, and Mi knew what syncytin did. The two other retroviral genes next to syncytin, gag and pol , were completely non-functional, McCoy says. Only env remained intact. The team published a paper in Nature in All mammals have placentas, including marsupials and egg-laying mammals. The syncytin produced by mice is completely different from the two syncytins found in humans and other primates.

At numerous points in mammalian evolution, symbiotic retroviruses entered the genome and steered different groups of mammals along different evolutionary paths, according to a paper in PNAS by virologist Harmit Malik at the Fred Hutchinson Cancer Research Center in Seattle.

Nor was syncytin the only driver. Renee Reijo Pera, a developmental biologist and embryonic stem cell expert then at Stanford University, had spent nearly two decades trying to understand how pluripotent embryonic stem cells—which have the ability to become any cell type—mature into their specialized adult forms.

Through hints from other animals, she realized that symbiotic viruses were a perfect candidate for this job. Even tiny shifts to the timing of certain developmental events could create large changes.