One of the theories how organisms switched from RNA to DNA is due to viruses. Viruses have a pretty wild range of their genetic diversity. Single strand DNA, double strand DNA, positive sense single strand RNA, negative sense single strand RNA, double strand RNA. We’ve also probably got viruses as a permanent part of our genome from some ancestor species.
I think they’re pretty cool. Also, they do respond to outside stimuli, otherwise they’d be completely inert.
We’ve also probably got viruses as a permanent part of our genome from some ancestor species.
We definitely have viruses as a permanent part of our genome. A type of herpes virus is present in the DNA of all living things descended from bony fishes
Mammals wouldn’t have a chorioallantoic placenta at all if not for a virus integrated into our genome. Mapping when in evolution the genes responsible for placental development first appeared was my first participation in scientific research, so I love this topic.
Happily! Basically, the true placenta we mammals (Eutheria) have is what allows such a long gestation period. Unlike our closely related marsupials, that quickly deplete their resources and must give birth, our placenta allows for a continuous exchange of nutrients. This involves a quite complicated process of embryonic tissue invading the uterine wall, so you can imagine the kind of immunological regulation that must be taking place for that to work.
So you’d assume we have several genes highly specific to our placenta that appear when we Eutherians first appeared… right? No! Turns out the vast majority already existed in jawed vertebrates (our common ancestor with sharks), then quite a lot show up in bony fish (our common ancestor with most things you call fish), and just one shows up in Tetrapoda (our common ancestor with amphibians).
So most of the framework for developing an organ such as the placenta already existed for millions of years, so what exactly was missing before it could finally show up in evolutionary history? The two genes that are absolutely required for this whole crazy “let’s invade the mother’s uterine wall tissue but NOT trigger her immune system” part: CSF2 and a group of closely related genes called syncitins.
Syncitins are the star here, because they’re actually a gene that came from ancient retroviruses. In the virus, they were expressed in the envelope and controlled the fusion between the viral particle and the host cell. These viruses got integrated into our genome, and this “fusion with the host cell” mechanism became extremely useful and crucial for the placenta, basically allowing it to exist.
Basically, yes. Viruses came up with the syncitins to fuse with host cells, then when they infected us and integrated their genome we had the code for making these proteins… and turns out “invading tissue” was a really useful tool for the embryo.
That’s a fantastic question… which is exactly what I’m pursuing in my master’s degree right now :). The goal will be to have a full metabolic map showing all the involved genes and how they interact, when they’re triggered (and by which signaling pathways) and how it all comes together for placental development.
They respond because they have to do things like inject the genetic material into the organism once it latches on to whatever on the cell surface. That doesn’t occur in the host, it occurs in the virus.
It’s been a while since I took virology, but I feel pretty confident that something occurs in the virus due to an external stimulus.
One of the theories how organisms switched from RNA to DNA is due to viruses. Viruses have a pretty wild range of their genetic diversity. Single strand DNA, double strand DNA, positive sense single strand RNA, negative sense single strand RNA, double strand RNA. We’ve also probably got viruses as a permanent part of our genome from some ancestor species.
I think they’re pretty cool. Also, they do respond to outside stimuli, otherwise they’d be completely inert.
We definitely have viruses as a permanent part of our genome. A type of herpes virus is present in the DNA of all living things descended from bony fishes
Mammals wouldn’t have a chorioallantoic placenta at all if not for a virus integrated into our genome. Mapping when in evolution the genes responsible for placental development first appeared was my first participation in scientific research, so I love this topic.
explain please
Happily! Basically, the true placenta we mammals (Eutheria) have is what allows such a long gestation period. Unlike our closely related marsupials, that quickly deplete their resources and must give birth, our placenta allows for a continuous exchange of nutrients. This involves a quite complicated process of embryonic tissue invading the uterine wall, so you can imagine the kind of immunological regulation that must be taking place for that to work.
So you’d assume we have several genes highly specific to our placenta that appear when we Eutherians first appeared… right? No! Turns out the vast majority already existed in jawed vertebrates (our common ancestor with sharks), then quite a lot show up in bony fish (our common ancestor with most things you call fish), and just one shows up in Tetrapoda (our common ancestor with amphibians).
So most of the framework for developing an organ such as the placenta already existed for millions of years, so what exactly was missing before it could finally show up in evolutionary history? The two genes that are absolutely required for this whole crazy “let’s invade the mother’s uterine wall tissue but NOT trigger her immune system” part: CSF2 and a group of closely related genes called syncitins.
Syncitins are the star here, because they’re actually a gene that came from ancient retroviruses. In the virus, they were expressed in the envelope and controlled the fusion between the viral particle and the host cell. These viruses got integrated into our genome, and this “fusion with the host cell” mechanism became extremely useful and crucial for the placenta, basically allowing it to exist.
Thanks for talking about that, that’s really cool!
That is nuts and a really good explaination, thank you!
So, in other words, viruses did parts of the work of evolution by inventing the CSF2 and syncitin genes?
And that regulates the immune system to not respond to foreign tissue?
Basically, yes. Viruses came up with the syncitins to fuse with host cells, then when they infected us and integrated their genome we had the code for making these proteins… and turns out “invading tissue” was a really useful tool for the embryo.
i am wondering (in case you know), what activates these genes?
i.e., i’d like to understand how gene regulation works in general. what causes genes to become active all of a sudden?
i.e., why does the genes allow embryos to live inside the mother, but not allow other intruders to live inside the human?
That’s a fantastic question… which is exactly what I’m pursuing in my master’s degree right now :). The goal will be to have a full metabolic map showing all the involved genes and how they interact, when they’re triggered (and by which signaling pathways) and how it all comes together for placental development.
I vaguely remember something about organelles inside a cell used to be seperate entities too
Mitochondria, for sure. They even still have their own DNA separate from your actual human DNA.
Yeah but they didn’t use to be viruses, they used to be bacteria.
And they didn’t integrate into human genome. They’re just another foreign body that lives inside human cells, but they have their own genome still.
Can you send the paper? Please. 🥺
Do they actually respond? Or is it the external stimuli responding to them?
They respond because they have to do things like inject the genetic material into the organism once it latches on to whatever on the cell surface. That doesn’t occur in the host, it occurs in the virus.
It’s been a while since I took virology, but I feel pretty confident that something occurs in the virus due to an external stimulus.