The kinetics of transposable element autoregulation.
Kinetic modeling of the self-regulatory mechanisms of transposable elements (TEs) involving interactions of one or a few gene products makes predictions that are often at odds with observed results. In particular, explanations 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 corresponding kinetic models. This is also true for similar mRNA-mRNA binding models. Self-repression in mariner as well as other TEs can, however, be explained 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 presence of divergent nonautonomous elements, since nondivergent monomers would be required at both TE ends for transposition.
Townsend
J P
JP
Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA.
Hartl
D L
DL
D000818:Animals; D004251:DNA Transposable Elements / Q000235:genetics* / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000235:genetics / Q000378:metabolism; D004926:Escherichia coli / Q000235:genetics / Q000378:metabolism; D006706:Homeostasis; D007700:Kinetics; D008954:Models, Biological; D012323:RNA Processing, Post-Transcriptional; D012329:RNA, Bacterial / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D019895:Transposases
D004251:DNA Transposable Elements; D004268:DNA-Binding Proteins; D012329:RNA, Bacterial; D012333:RNA, Messenger; C111652:mariner transposases; D019895:Transposases