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.
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.