Transposition of Tn10 requires sites at the termini of the element and one essential transposon-encoded function, "transposase", which acts at those termini. Genetic complementation experiments reveal that this "transposase" function works much more efficiently on transposon ends located near the gene from which they are expressed than on transposon ends located at a distance. This property accounts for the failure of mutant Tn10 elements to be efficiently complemented in trans. The failure of transposase protein to move freely in three dimensions could be explained by one-dimensional diffusion, energy-dependent translocation and/or extreme protein lability. Additional genetic analyses demonstrate that the rate of Tn10 transposition in vivo depends upon the length of the transposon and the amount of transposase protein. Function dependence and length dependence are independent aspects of the transposition process that could correspond to the break/join and replication aspects into which transposition has been separated conceptually.