Analysis of sequences transposed by complementation of two classes of transposition-deficient mutants of Tn3

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Abstract
The Tn1 and Tn3 elements are closely related transposons which carry the structural gene for ampicillin resistance [in Escherichia coli]. Two classes of deletion mutants of the plasmid pMB8::Tn3 (RSF1050) are unable to transpose ampicillin resistance but can be complemented in trans by a coresident Tn1 or Tn3 element. The analysis of the sequences transposed upon complementation of 1 class of mutants (type I) showed that the mutant element had undergone bona fide transposition. Complementation of the type II mutants led to the transposition of a sequence analogous to bacteriophage mu-promoted integration of non-mu DNA. The transposed sequence consisted of 2 Tn3 elements which flanked a single copy of the pMB8 portion of the RSF1050 genome. Complementation data indicated that the type II mutants are defective in at least 1 trans-acting function which must be supplied for transposition to occur. The nature of the sequence-transposed from the type II mutant is the consequence of a defective cis-acting function (or site). The type II mutants were defective in a trans-acting function which regulated the frequency of transposition.