SUMMARY: It was concluded in the preceding paper that λ I genomes probably failed to form plasmids within infected cells because they leakily express functions that act to destabilize the plasmid state. This prediction was investigated by examining the effect upon plasmid-forming ability of the loss of possible anti-plasmid functions. The loss of Ter function was found to allow long-term plasmid formation, although the efficiency of initial plasmid formation and the heritable stability without selection were low. The combined loss of the and gene functions also promoted plasmid growth, although the absence of Terλ was necessary. In contrast, the presence of Ter (due to an substitution) did not prevent plasmid formation when the and genes were absent, indicating that Ter does not attack the closed-circular form of the λ chromosome. The combined loss of the and gene functions facilitated fully efficient inheritance of the λ I plasmids in the absence of selection, although the efficiency of initial plasmid formation remained low. However, cells harbouring such plasmids suffered a decline in viability, indicating that the plasmids expressed a function (or more than one) that acts to debilitate the host cells - presumably an effect that is increased with this genotype because the modified λ I plasmids are inherently more stable. The possible involvement of the λ and functions in destabilization is discussed.


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