Transposition of DNA inserted into deletions of the Tn5 kanamycin resistance element.
Tn5-trp hybrid transposons have been constructed by insertion of a trpPOED Hind III fragment into an in vivo Tn5 internal deletion mutant or by substitution of trp for the internal Tn5 Hind III fragment. These hybrids are called, respectively, Tn409 and Tn410. Both Tn409 and Tn410 will transpose into lambda in the presence of a complementing Tn5 element. In the absence of a wild Tn5, lysogens carrying R1162::Tn409 and R1162::Tn410 plasmids will yield lambdatrp phages at less than six per cent of the complemented frequency. This reduction indicates that Tn409 and Tn410 lack a diffusible transposition function provided by wild Tn5 elements. However, the formation of lambdatrp phages without complementation is real. Most of these transducing particles contain Tn409 and Tn410 still linked to the carrier R1162 plasmid. This observation suggests that uncomplemented Tn409 and Tn410 elements mediate the formation of lambda-transposon-plasmid cointegrate structures. Thus, the missing transposition function may be involved in resolving these cointegrate structures to the final lambda::Tn409 or lambda::Tn410 product.
D002874:Chromosome Mapping; D003090:Coliphages / Q000187:drug effects / Q000235:genetics*; D004279:DNA, Viral / Q000235:genetics*; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics; D005816:Genetic Complementation Test; D007612:Kanamycin / Q000494:pharmacology*; D008242:Lysogeny; D009876:Operon; D011815:R Factors; D011995:Recombination, Genetic; D014161:Transduction, Genetic
D004279:DNA, Viral; D007612:Kanamycin