Abstract
Mutations of Tn5 which decreased the amount of the shorter element-encoded protein (p2) were made. One mutation was a change in the translation initiation codon of the protein, while two other mutations were changes in the promoter of the transcript (T2) which codes for p2. Analysis of all three mutants indicates that they decreased the inhibition of transposition that the protein exerts (in trans) on another element. The mutants have complicated transposition behaviors. Analysis of the RNA and proteins synthesized from the mutants led to the proposal that p2 can inhibit transposition at normal physiological concentrations. Therefore p2 synthesized from a given element is partly responsible for controlling the transposition frequency of the element. The mutants also show that p1 is the only Tn5-encoded protein necessary for transposition.