Plasmid incompatibility and control of replication: copy mutants of the R-factor R1 in Escherichia coli K-12.
Plasmid incompatibility was studied in Escherichia coli K-12. By double-antibiotic selection, clones were constructed that carried the two R-factors R1 and R100, both belonging to the compatibility group FII. After release of the selection pressure, each of the two plasmids was lost at the same rate (8% per generation). Mutants of R-factor R1 showing an increased number of copies per chromosome (copy mutants) were tested for their incompatibility towards R-factor R100. The results indicate that plasmid incompatibility is quantitative and not just a qualitative property. All copy mutants studied affected incompatibility, and there were two classes of mutants: one increasing and one decreasing the incompatiblity exerted towards the test plasmid R100. Evidence is presented that incompatibility is related to the mechanisms that control replication. The implications of such a relation on proposed models for control of replication are discussed. The data do not support the hypothesis that plasmid incompatibility is due to competition for a replicational or segregational site.
D000667:Ampicillin / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D003227:Conjugation, Genetic; D004261:DNA Replication; D004269:DNA, Bacterial / Q000096:biosynthesis; D004926:Escherichia coli / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D007612:Kanamycin / Q000494:pharmacology; D009154:Mutation; D010403:Penicillin Resistance; D010405:Penicillinase / Q000096:biosynthesis; D011815:R Factors
D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D007612:Kanamycin; D000667:Ampicillin; D010405:Penicillinase