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The role of the recA and rnhA mutations on the growth of different thermo-sensitive mutants at the non permissive temperature was studied. The growth of Hfr strains selected by integrative suppression in a dnaA(Ts) mutant was found strongly dependent on the RecA protein. This latter gene product was also essential for gyrA(Ts) and gyrB(Ts), rnhA double mutants for growing at 43°C. This RecA+ dependent cell multiplication was due to the fact that all the strains studied initiated their DNA synthesis from site(s) different from the normal gene oriC. This phenomenon causes in the cell a non-stop production of the bacterial genome with concomitant disorders in the bacterial division process. It has been suggested that when the growth of the microorganism is driven by an extra-chromosomal genetic element it behaves like a transformed tumor cell. Thus the bacterial model may present many advantages for studying the mechanisms by which cells lose the control of their division process because of an infecting foreign genetic element integrated in their chromosome.

The peculiar behavior of dnaA, gyrA and gyrB temperature-sensitive mutants and their Hfr derivatives made recA, rnhA or both mutants