Transposons activity is not downregulated in the placenta while being downregulated in most other cells. If there are too many transposons in the DNA that likely makes the placenta fail during the pregnancy. As a result, the amount of variance in transposon counts you see when sequencing born people is more limited than that of embryos.
If you do IVF you care about the pregnancy not terminating after three or four months.
The evidence is more of a theoretical argument. In the selfish gene frame, transposons (even when they aren’t technically genes) “benefit” from copying themselves even when it reduces the total fitness of the organism.
You need a mechanism that prevents people with too many transposons from procreating to account for transposons counts not just growing indefinitely.
In the absence of a process that regulates a quantity, you have variance. Lack of observed variance in sequenced adult genomes is evidence of a mechanism for regulation existing.
Transposons activity is not downregulated in the placenta while being downregulated in most other cells. If there are too many transposons in the DNA that likely makes the placenta fail during the pregnancy. As a result, the amount of variance in transposon counts you see when sequencing born people is more limited than that of embryos.
If you do IVF you care about the pregnancy not terminating after three or four months.
The evidence is more of a theoretical argument. In the selfish gene frame, transposons (even when they aren’t technically genes) “benefit” from copying themselves even when it reduces the total fitness of the organism.
You need a mechanism that prevents people with too many transposons from procreating to account for transposons counts not just growing indefinitely.
In the absence of a process that regulates a quantity, you have variance. Lack of observed variance in sequenced adult genomes is evidence of a mechanism for regulation existing.