@article {540086,
	title = {The kinetics of transposable element autoregulation},
	journal = {Genetica},
	volume = {108},
	number = {3},
	year = {2000},
	note = {<p>Townsend, J PHartl, D LengResearch Support, U.S. Gov{\textquoteright}t, P.H.S.Netherlands2001/04/11 10:00Genetica. 2000;108(3):229-37.</p>},
	pages = {229-37},
	abstract = {<p>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.</p>},
	keywords = {*Models, Biological, Animals, DNA Transposable Elements/*genetics/*physiology, DNA-Binding Proteins/genetics/metabolism, Drosophila melanogaster/genetics/metabolism, Escherichia coli/genetics/metabolism, Homeostasis, Kinetics, RNA Processing, Post-Transcriptional, RNA, Bacterial/genetics/metabolism, RNA, Messenger/genetics/metabolism, Transposases},
	isbn = {0016-6707 (Print)0016-6707 (Linking)},
	author = {Townsend, J. P. and Hartl, D. L.}
}
