(I made an account to post this)
We do have mechanisms to repress transposon activity, most notably epigenetic mechanisms. Most DNA is usually tightly coiled up around little cylindrical proteins (called histones), where it can’t be easily transcribed. “Epigenetics” typically refers to modifications of the DNA and/or histones which make the coils tighter or looser, making the DNA difficult or easy to access. Most transposons are epigenetically tagged so that they’re kept tightly coiled most of the time.
These mechanisms are small interfering RNAs (siRNAs) and Piwi-interacting RNAs (piRNAs), that increase methylation of the histones associated with transposons, making them ‘tighter’, or harder to access. According to the Wikipedia page for transposon silencing, these siRNAs and piRNAs are most active in the gonads. This makes sense, as it would avoid germline transmission of active transposons, allowing offspring to be born with a lower active transposon count than their parents.
After reading that, I wondered why on earth we don’t have these transposon-suppressing RNAs coursing through our bloodstream in the same concentration as we do in our gonads. According to this paper, suppressing transposons also has the effect of suppressing neighboring genes, leading to a possible reduction in the organism’s fitness. The same paper claims that having transposons could have beneficial effects on genome evolution, as transposons create regions of suppressed recombination around them, although I don’t fully understand the reasoning behind this being good for organism fitness. Also, if suppressing transposons does have negative effects on the genome, that doesn’t at all explain why it happens more in the gonads. Perhaps aging just wasn’t selected against enough in the ancestral environment.
If nothing else, these siRNAs and piRNAs seem to be effective at making babies have fewer active transposons than their parents. If someone has injected old mice with a bunch of copies of these RNAs (probably wrapped in viruses first) and observed the results, then I can’t find their paper published anywhere. On the off chance that the transposon model is correct, and that the cure for transposon proliferation really is as simple as an RNA injection, this is one experiment we can’t afford not to do.
This advice is probably good in most social contexts—but I really appreciate the rationalist norm of taking deception very seriously. I resolve this class of conflict by being much more apprehensive than usual about casually misleading my rationalist-adjacent friends and business associates.