Transposons increase the mutation rate, so the fitness of organisms changes more when there are transposons in my model. When it comes to that I treat every transposons equally. Otherwise, each transposon has a rate for self replication. Aside of that transposons have no positive benefits but they self reproduce. If the mutation rate is what’s useful then there should be pressure for transposons with low self replication rates which I don’t see.
Transposons work similar to the gene drive ideas for killing of malaria causing mosquitos.
However the body does have some defenses. Both the transposons evolve and the defenses evolve and in nature there’s an equilibrium.
Finding the right parameters that lead to the equilibrium, might produce a model that does predict aging purely based on the fact that transposons exist.
From what I read evolutionary models generally don’t need group selection to work. If transposons kill every species if it wouldn’t be for group selection that would be a major scientific finding.
There’s the belief that the minimum number of individuals for a specis is 500 over longer timeframes.
This is why it would make sense if there was some (perhaps small) positive effect of transposons on an individual’s fitness.
(Also, aren’t there any less costly ways to increase mutation rate? Maybe error-prone DNA polymerases, or just allocating less resources to DNA repair.)
Also, aren’t there any less costly ways to increase mutation rate?
It’s not costly for a transposon to copy itself. If you start a gene drive to erradicate malaria, it’s not in the interest of the individual mosquito to play along but it still happens.
A positive selective effect of transposon on the level of the individual is not needed for transposons to have a reason to copy themselves. I’m doing computer modeling and the question of what stops transposons is a harder one then the other way around.
Aside from that it seems that humans do use the fact that the have transporase for a few things (but currently not in my computer model). PGBD5 (a transporase) seems to be used in the brain to increase the diversity of brain cells for all vertebrates since 500 My.
RAG1 and RAG2 are derived from a transporase and they are important in the immune system to get a diversity of different leukozytes.
This means that neither of those can be completely downregulated and when they are active transposons can use them to get copied around.
An interesting side-note is human have a lot of different kinds of cells where some cells get cancer much more frequently then others.
Leukemia is a common cancer and might be downstream from RAG1 / RAG2. Braincancer might be downstream from PGBD5.
Most childhood cancers are downstream from PGBD5 as well, so it’s the most costly transporase for fitness.
I’m playing around with an evolutionary model for transposons and the transposons regularly kill my whole population...
Do the transposons ever have positive benefits?
Why is your population all connected?
Transposons increase the mutation rate, so the fitness of organisms changes more when there are transposons in my model. When it comes to that I treat every transposons equally. Otherwise, each transposon has a rate for self replication. Aside of that transposons have no positive benefits but they self reproduce. If the mutation rate is what’s useful then there should be pressure for transposons with low self replication rates which I don’t see.
Transposons work similar to the gene drive ideas for killing of malaria causing mosquitos.
However the body does have some defenses. Both the transposons evolve and the defenses evolve and in nature there’s an equilibrium.
Finding the right parameters that lead to the equilibrium, might produce a model that does predict aging purely based on the fact that transposons exist.
Having such a theory would back up https://www.lesswrong.com/posts/ui6mDLdqXkaXiDMJ5/core-pathways-of-aging .
From what I read evolutionary models generally don’t need group selection to work. If transposons kill every species if it wouldn’t be for group selection that would be a major scientific finding.
There’s the belief that the minimum number of individuals for a specis is 500 over longer timeframes.
This is why it would make sense if there was some (perhaps small) positive effect of transposons on an individual’s fitness.
(Also, aren’t there any less costly ways to increase mutation rate? Maybe error-prone DNA polymerases, or just allocating less resources to DNA repair.)
It’s not costly for a transposon to copy itself. If you start a gene drive to erradicate malaria, it’s not in the interest of the individual mosquito to play along but it still happens.
A positive selective effect of transposon on the level of the individual is not needed for transposons to have a reason to copy themselves. I’m doing computer modeling and the question of what stops transposons is a harder one then the other way around.
Aside from that it seems that humans do use the fact that the have transporase for a few things (but currently not in my computer model). PGBD5 (a transporase) seems to be used in the brain to increase the diversity of brain cells for all vertebrates since 500 My.
RAG1 and RAG2 are derived from a transporase and they are important in the immune system to get a diversity of different leukozytes.
This means that neither of those can be completely downregulated and when they are active transposons can use them to get copied around.
An interesting side-note is human have a lot of different kinds of cells where some cells get cancer much more frequently then others.
Leukemia is a common cancer and might be downstream from RAG1 / RAG2. Braincancer might be downstream from PGBD5.
Most childhood cancers are downstream from PGBD5 as well, so it’s the most costly transporase for fitness.