Enhanced instability of IncFII basic replicon by the polA mutation.
IncFII plasmids consisting of a basic replicon and of an additional fragment(s) unrelated to plasmid maintenance were all less stable in polA1 than in its wild type. Reversion to UV-resistance recovered stability and vice versa. UV irradiation promoted instability in polA1 cells. Larger plasmids showed a greater instability and a fewer number of copies in a same host. Surprisingly, polA1 cells with Tn3 on the plasmid showed a higher ampicillin resistance than the wild type, apparently suggesting that the polA1 mutation increases the copy number. The size-dependency of instability was less marked in polA1 than in its parent. Comparison of the generation times has suggested a detrimental effect exerted by a basic replicon in polA1 hosts.
D000667:Ampicillin / Q000494:pharmacology; D001435:Bacteriophages / Q000235:genetics* / Q000528:radiation effects; D004262:DNA Restriction Enzymes / Q000378:metabolism; D004279:DNA, Viral / Q000032:analysis; D015246:Deoxyribonuclease EcoRI; D009154:Mutation; D010403:Penicillin Resistance; D010957:Plasmids; D012093:Replicon; D014466:Ultraviolet Rays
D004279:DNA, Viral; D000667:Ampicillin; D004262:DNA Restriction Enzymes; D015246:Deoxyribonuclease EcoRI