The evolution of self-regulated transposition of transposable elements.

This paper examines the conditions under which self-regulated rates of transposition can evolve in populations of transposable elements infecting sexually reproducing hosts. Models of the evolution of both cis-acting regulation (transposition immunity) and trans-acting regulation (transposition repression) are analyzed. The potential selective advantage to regulation is assumed to be derived from the deleterious effects of mutations associated with the insertion of newly replicated elements. It is shown that both types of regulation can easily evolve in hosts with low rates of genetic recombination per generation, such as bacteria or bacterial plasmids. Conditions are much more restrictive in organisms with relatively free recombination. In haploids, the main selective force promoting regulation is the induction of lethal or sterile mutations by transposition; in diploids, a sufficiently high frequency of dominant lethal or sterile mutations associated with transpositions is required. Data from Drosophila and maize suggest that this requirement can sometimes be met. Coupling of regulatory effects across different families of elements would also aid the evolution of regulation. The selective advantages of restricting transposition to the germ line and of excising elements from somatic cells are discussed.