The kinetics of transposable element autoregulation

Kinetic modeling of the sell-regulatory mechanisms of transposable elements (TEs) involving interactions of one or a few gene products makes predictio ns that are often at odds with observed results. In particular, explanation s of TE autorepression at high copy number that invoke a decrease in number of active monomers through dimerization, amyloidization, and protein-mRNA binding to create an inactive state are not supported by analysis of the co rresponding kinetic models. This is also true for similar mRNA-mRNA binding models. Self-repression in mariner as well as other TEs can, however, be e xplained by a host-independent model in which inactive dimers compete with monomers for TE binding sites at the ends of the element. This model would also allow heterodimer poisoning to down-regulate transposition in the pres ence of divergent nonautonomous elements, since nondivergent monomers would be required at both TE ends for transposition.