ISSN:
1573-6857
Keywords:
autoregulation
;
dimerization
;
kinetics
;
post-transcriptional regulation
;
transposable elements (TEs)
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
Notes:
Abstract 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 marineras 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1004172703790
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