not sure if I'm following exactly, but you seem to have to assume the duplication event itself is adaptive, right? If amount of noncoding DNA correlates with number of gene duplications, maybe you've just discovered that duplications can include things other than genes, which might not be all that interesting.

Well, the idea here was that adaptive gene duplications should correlate with spurts of retrotranspositional amplification. So there'd need to be some way to trace the history of the latter, and I don't really know how that would be done.

Probably a moot point, though: having looked into it, this doesn't work the way I thought it would. I knew that LINEs sometimes end up dragging some of the host's genetic material along in their replications, but now I know that the way this happens is that sometimes the reverse-transcription machinery grabs onto host mRNA that's floating around and splices it in. So what's being inserted is automatically a pseudogene since the mRNA has already been processed (i.e. there's no promoter attached to it). For this idea to work it would need to be an active gene. Rats.

Mind you, DNA transposons could still easily easily be a major source of gene duplication since they skip the RNA middleman. But since they're only a tiny fraction of ncDNA that means it probably has nothing to do with the C-value enigma.

DNA transposons could still easily easily be a major source of gene duplication since they skip the RNA middleman.

LTRs (left behind by transposition) are known sites of gene duplication and deletion events, possible due to non-allelic homologous recombination. I don't think this mechanism works in your model, though.