Molecular Biology and Evolution, Vol 13, 549-555, Copyright © 1996 by Society for Molecular Biology and Evolution
AR Lohe and DL Hartl
Genetic studies of the mariner transposable element Mos1 have revealed two
novel types of regulatory mechanisms. In one mechanism, overproduction of
the wild-type transposase reduces the overall level of transposase activity
as assayed by the excision of a nonautonomous mariner target element. This
mechanism is termed overproduction inhibition (OPI). Another mechanism is
observed in a class of hypomorphic missense mutations in the transposase.
In the presence of wild-type Mos1 transposase, these mutations exhibit
dominant-negative complementation (DNC) that antagonizes the activity of
the wild-type transposase. We propose that these regulatory mechanisms act
at the level of the transposase protein subunits by promoting the assembly
of oligomeric forms, or of mixed-subunit oligomers, that have reduced
activity. We suggest that these regulatory mechanisms may apply generally
to mariner-like elements (MLEs). Overproduction inhibition may help explain
why the MLE copy number reaches very different levels in different species.
Dominant-negative complementation may help explain why most naturally
occurring copies of MLEs have been mutationally inactivated.
ORIGINAL ARTICLE
Autoregulation of mariner transposase activity by overproduction and dominant-negative complementation
Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA. d_hartl@harvard.edu
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