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Pairs of normally incompatible derivatives of R100-1 (one Chls TetR, the other ChlRTets) were forced to coexist in a recA host by selection for ChlR TetR cells. After many generations stable derivatives were isolated. The analysis of nine independent stabilization experiments showed that in each case TetR was translocated from the plasmid to the chromosome of the host. No evidence for the joint integration of other plasmid genes (those controlling transfer, antibiotic resistance, incompatibility, or origin of transfer replication) was obtained. One of the chromosomal TetR determinants was mapped close to metE.

Deletions in the tet genes derived from TnJO were formed from different tet::TnS insertion mutations by removing DNA sequences located between a HindIII site in TnS and a HindIII site adjacent to the tet genes. Tetracyclinesensitive point mutations were mapped in recombination tests with the deletions and were thus aligned with the genetic and physical map of the tet region.Plasmids carrying point mutations were tested for complementation with derivatives of pDU938, a plasmid carrying cloned tet genes derived from TnJO which had been inactivated by Tn5 insertions. Complementation occurred between promoter-proximal tet point mutations and distal tet::TnS insertions, suggesting the existence of two structural genes, tetA and tetB. These results, together with the analysis of polypeptides in minicells harboring pDU938tet::TnS mutants,

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