Genome sequencing has revealed a tremendous diversity of transposable elements (TEs) in eukaryotes but there is little understanding of the evolutionary processes responsible for TE diversity. Non-autonomous TEs have lost the machinery necessary for transposition and rely on closely related autonomous TEs for critical proteins. We studied two mathematical models of TE regulation, one assuming that both autonomous tranposons and their non-autonomous relatives operate under the same regulatory logic, competing for transposition resources, and one assuming that autonomous TEs self-attenuate transposition while non-autonomous transposons continually increase, parasitizing their autonomous relatives. We implemented these models in stochastic simulations and studied how TE regulatory relationships influence transposons and populations. We found that only outcrossing populations evolving with Parasitic TE regulation resulted in stable maintenance of TEs. We tested our model predictions in Caenorhabditis genomes by annotating TEs in two focal families, autonomous LINEs and their non-autonomous SINE relatives and the DNA transposon Mutator. We found broad variation in autonomous - non-autonomous relationships and rapid mutational decay in the sequences that allow non-autonomous TEs to transpose. Together, our results suggest that individual TE families evolve according to disparate regulatory rules that are relevant in the early, acute stages of TE invasion.
