AUTOREGULATION OF MARINER TRANSPOSASE ACTIVITY BY OVERPRODUCTION AND DOMINANT-NEGATIVE COMPLEMENTATION

Genetic studies of the mariner transposable element Mos1 have revealed two novel types of regulatory mechanisms. In one mechanism, overprodu ction of the wild-type transposase reduces the overall level of transp osase activity as assayed by the excision of a nonautonomous mariner t arget element. This mechanism is termed overproduction inhibition (OPI ). Another mechanism is observed in a class of hypomorphic missense mu tations in the transposase. In the presence of wild-type Mos1 transpos ase, these mutations exhibit dominant-negative complementation (DNC) t hat antagonizes the activity of the wild-type transposase. We propose that these regulatory mechanisms act at the level of the transposase p rotein subunits by promoting the assembly of oligomeric forms, or of m ixed-subunit oligomers, that have reduced activity. We suggest that th ese regulatory mechanisms may apply generally to mariner like elements (MLEs). Overproduction inhibition may help explain why the MLE copy n umber reaches very different levels in different species. Dominant-neg ative complementation may help explain why most naturally occurring co pies of MLEs have been mutationally inactivated.