SELFISH RESTRICTION-MODIFICATION GENES - RESISTANCE OF A RESIDENT R MPLASMID TO DISPLACEMENT BY AN INCOMPATIBLE PLASMID-MEDIATED BY HOST KILLING/

Previous work from this laboratory demonstrated that plasmids carrying a type II restriction-modification gene complex are not easily lost f rom their bacterial host because plasmid-free segregant cells are kill ed through chromosome cleavage, Here, we have followed the course of e vents that takes place when an Escherichia coli recBC sbcA strain carr ying a plasmid coding for the PaeR71 restriction-modification (R/M) ge ne complex is transformed by a plasmid with an identical origin of rep lication, The number of transformants that appeared was far fewer than with the restriction-minus (r(-)) control, Most of the transformants were very small, After prolonged incubation, the number and the size o f the colonies increased, but this increase never attained the level o f the r(-) control. Most of the transformed colonies retained the drug -resistance of the resident, r(+) m(+) plasmid, These results indicate that post-segregational host killing occurs when a plasmid bearing an R/M gene complex is displaced by an incompatible plasmid. Such cell k illing eliminates the competitor plasmid along with the host and, thus , would allow persistence of the R/M plasmid in the neighboring, clona l host cells in nature. This phenomenon is reminiscent of mammalian ap optosis and other forms of altruistic cell death strategy against infe ction. This type of resistance to displacement was also studied in a w ild type Escherichia coli strain that was normal for homologous recomb ination (rec(+)). A number of differences between the recBC sbcA strai n and the rec(+) strain were observed and these will be discussed.