spacemonkeymafia42 t1_j9nfn1v wrote on February 23, 2023 at 5:34 AM

Reply to comment by fil- in How did the placenta evolve? by fil-

There's evidence that a gene responsible for placental development in humans came from an ancient virus!

Syncytin-1, a protein coded by the ERV1 gene which is crucial for placental development. Syncytin-1 is a human endogenous retroviral element, viral genetic material that has incorportated into our genome. It is conserved among apes and old-world monkeys.

Syncytin-2, another placental development gene, is derived from a different retrovirus.

unconventionally_ t1_j9nleic wrote on February 23, 2023 at 6:37 AM

Whoa. How do we adapt virus genes into our DNA? I’m so intrigued

joalheagney t1_j9nr2t2 wrote on February 23, 2023 at 7:47 AM

Keeping it short? Viruses reproduce by inserting DNA into our cells' nuclei (Even the RNA viruses - there's just extra steps).

Several viruses have a dormant stage, where they infect a cell, but don't produce new viral particles unless triggered - usually by stress of the host. Herpes simplex is a good example, which is why cold sores come back.

Once a viral gene is in a stem cell, it's up for reuse and adaptation via evolution, just like any other gene.

[deleted] t1_j9pbykb wrote on February 23, 2023 at 4:49 PM

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djublonskopf t1_j9oso0h wrote on February 23, 2023 at 2:43 PM

Specifically, the syncytins are important because they keep the mother's immune cells from being able to reach "through" the placenta into the developing fetus.

There are certain immune cells that are able to slip between other epithelial cells. If the mother's immune cells were to slip past the cells of placenta, they would almost certainly attack the fetus. Placental mammals solve this by having a "boundary layer" between the placenta and the mother. The cells of the boundary layer use those viral syncytins to "fuse" together, becoming one giant solid mega-cell with lots of nuclei. Because there are no longer any individual cells to slip between, the mother's immune cells are unable to get past this boundary layer (the syncytiotrophoblast) and thus the rest of the placenta and fetus are protected from the mother's immune system.