https://science.thewire.in/the-sciences/why-humans-dont-lay-eggs-a-viral-story/

"In 2011, a team of scientists led by the paleontologist Zhe-Xi Luo discovered a well-preserved fossil from North-east China that will push back the timeline of the emergence of a very important group of animals by 35 million years to 160 million years ago. Named Juraimaia sinesis i.e., the Jurassic mother from China, the fossil revealed a shrew-like mammal, barely 100 mm in length, that had walked upon the Earth alongside the gigantic dinosaurs of the Jurassic era.
....
It has been argued by diverse groups of researchers that in a harsh Jurassic environment strewn with ferocious predators, Juramaia and its offspring would not have had a fair chance to thrive, if not for the placenta. The placenta allows for continuous nutrition supply, efficient exchange of respiratory gases, and a means for waste disposal in the live-bearing mammal.
....
The obvious question is whether acquiring the placenta is a once-in-a-million-years flash in the evolutionary pan, a genetic prerogative that empowered the ancestral Eutherians to get a head start on ensuring the survival of offspring. The answer surprisingly is no!
....
Soon after fertilisation, the embryo implants into the uterine wall, wherein all its future physiological demands will be met through the placenta that begins forming at about week four post-conception for humans. As the ball-like embryo attaches to the wall of the uterus, the outermost layer of this ball extends finger-like projections known as placental villi to invade the uterine tissue. A continuous layer of fused cells known as syncytiotrophoblasts line the outermost border of these finger-like villi and stand guard at the junction of the mother’s tissue with the fetal tissue. They act as the placental barrier ensuring nutrient and gas exchange occurs with the mother’s blood but nothing undesirable can get in from the maternal circulation to harm the embryo and the future fetus. Behind this critical ability of syncytiotrophoblasts to act as selective filter is the contribution of a unique gene and its encoded protein known as syncytin-1. In 1999, French researchers stumbled upon the origin of the syncytin-1 gene in human placenta and were amazed to find that the gene sequence showed a 100% match with the envelope protein of a human endogenous retrovirus known as HERV-W2. Further studies on laboratory mice subsequently revealed that if syncytin-1 is removed or inhibited, it will surely lead to the abortion of the foetus or cause embryonic death – thereby underlying the central role in mammalian reproduction.

Human endogenous retroviruses (HERVs) can be considered as fossil remains of ancient retroviruses (a family of viruses of which the most well-known representative is the human immunodeficiency virus type 1, which causes AIDS) which had infected our proto-placental ancestors. After gaining entry inside the host cell, retroviruses typically insert themselves into the host’s DNA, hijack the host’s cellular machinery to make thousands of copies of themselves, and then exit to infect more cells. During such an insertion event, it is likely that some ancient retroviruses lost their ability to multiply, eventually getting trapped inside the cells of the proto-placental ancestor and their genes consequently becoming a part of our DNA. Although the retroviruses of today are known to infect only bodily (somatic) cells, it is believed that in the past, they might have occasionally integrated into the germline DNA (DNA of eggs and sperms), enabling vertical transmission from one generation to the next.
....
So, how did our placental ancestors gain syncytin-1? Paleovirologists estimate that retroviruses started infecting vertebrates around 450 million years ago. Somewhere between 150 and 200 million years ago, an ancestor of HERV-W2 may have infected a proto-placental ancestor of Juramaia. During infection, this retrovirus infected cells in the germ line (eggs and sperms) and owing to some random mutation lost its ability to multiply or exit thereby becoming an endogenous retrovirus. Through millions of years of evolution, most of the genes of this retrovirus got silenced but one gene continued to be functional. This is the syncytin-1 gene, originally responsible for encoding envelope glycoproteins to help the virus ‘to fuse’ with the host cell during the initiation of infection. Having lost its ability to contribute to the viral life cycle, the function of syncytin-1 was repurposed for the development of a multi-nucleate tissue layer which separates maternal and fetal blood in placental circulation thereby ensuring the integrity of the developing embryo. "

You touching your dick ?

(While watching porn)

On Wednesday, July 26, 2023 at 9:02:52 AM UTC-4, ltlee1 wrote:
> https://science.thewire.in/the-sciences/why-humans-dont-lay-eggs-a-viral-story/
>
> "In 2011, a team of scientists led by the paleontologist Zhe-Xi Luo discovered a well-preserved fossil from North-east China that will push back the timeline of the emergence of a very important group of animals by 35 million years to 160 million years ago. Named Juraimaia sinesis i.e., the Jurassic mother from China, the fossil revealed a shrew-like mammal, barely 100 mm in length, that had walked upon the Earth alongside the gigantic dinosaurs of the Jurassic era.
> ...
> It has been argued by diverse groups of researchers that in a harsh Jurassic environment strewn with ferocious predators, Juramaia and its offspring would not have had a fair chance to thrive, if not for the placenta. The placenta allows for continuous nutrition supply, efficient exchange of respiratory gases, and a means for waste disposal in the live-bearing mammal.
> ...
> The obvious question is whether acquiring the placenta is a once-in-a-million-years flash in the evolutionary pan, a genetic prerogative that empowered the ancestral Eutherians to get a head start on ensuring the survival of offspring. The answer surprisingly is no!
> ...
> Soon after fertilisation, the embryo implants into the uterine wall, wherein all its future physiological demands will be met through the placenta that begins forming at about week four post-conception for humans. As the ball-like embryo attaches to the wall of the uterus, the outermost layer of this ball extends finger-like projections known as placental villi to invade the uterine tissue. A continuous layer of fused cells known as syncytiotrophoblasts line the outermost border of these finger-like villi and stand guard at the junction of the mother’s tissue with the fetal tissue. They act as the placental barrier ensuring nutrient and gas exchange occurs with the mother’s blood but nothing undesirable can get in from the maternal circulation to harm the embryo and the future fetus. Behind this critical ability of syncytiotrophoblasts to act as selective filter is the contribution of a unique gene and its encoded protein known as syncytin-1. In 1999, French researchers stumbled upon the origin of the syncytin-1 gene in human placenta and were amazed to find that the gene sequence showed a 100% match with the envelope protein of a human endogenous retrovirus known as HERV-W2. Further studies on laboratory mice subsequently revealed that if syncytin-1 is removed or inhibited, it will surely lead to the abortion of the foetus or cause embryonic death – thereby underlying the central role in mammalian reproduction.
>
> Human endogenous retroviruses (HERVs) can be considered as fossil remains of ancient retroviruses (a family of viruses of which the most well-known representative is the human immunodeficiency virus type 1, which causes AIDS) which had infected our proto-placental ancestors. After gaining entry inside the host cell, retroviruses typically insert themselves into the host’s DNA, hijack the host’s cellular machinery to make thousands of copies of themselves, and then exit to infect more cells. During such an insertion event, it is likely that some ancient retroviruses lost their ability to multiply, eventually getting trapped inside the cells of the proto-placental ancestor and their genes consequently becoming a part of our DNA. Although the retroviruses of today are known to infect only bodily (somatic) cells, it is believed that in the past, they might have occasionally integrated into the germline DNA (DNA of eggs and sperms), enabling vertical transmission from one generation to the next.
> ...
> So, how did our placental ancestors gain syncytin-1? Paleovirologists estimate that retroviruses started infecting vertebrates around 450 million years ago. Somewhere between 150 and 200 million years ago, an ancestor of HERV-W2 may have infected a proto-placental ancestor of Juramaia. During infection, this retrovirus infected cells in the germ line (eggs and sperms) and owing to some random mutation lost its ability to multiply or exit thereby becoming an endogenous retrovirus. Through millions of years of evolution, most of the genes of this retrovirus got silenced but one gene continued to be functional. This is the syncytin-1 gene, originally responsible for encoding envelope glycoproteins to help the virus ‘to fuse’ with the host cell during the initiation of infection. Having lost its ability to contribute to the viral life cycle, the function of syncytin-1 was repurposed for the development of a multi-nucleate tissue layer which separates maternal and fetal blood in placental circulation thereby ensuring the integrity of the developing embryo. "

We have retroviruses in the body. We also have mitochondria in the body.
One question now is whether we also have genes for photosynthesis as part of the junk DNA waiting to be active with high atmospheric CO2 level.