IS1-dependent generation of high-copy-number replicons from bacteriophage P1 Ap Cm as a mechanism of gene amplification.
Mutant P1 Ap Cm lysogens were isolated in which the drug resistance genes resident on the plasmid prophage P1 Ap Cm are amplified by a novel mechanism. The first step required for amplification is IS1-mediated rearrangement of the P1 Ap Cm prophage. The drug resistance genes are amplified from the rearranged P1 Ap Cm prophage by the formation of a plasmid (P1dR) which contains the two resistance genes. The P1dR plasmid is an independent replicon about one-half the size of P1 Ap Cm that can be maintained at a copy number eightfold higher than that at which P1 Ap Cm can be maintained. It contains no previously identified replication origin and is dependent on the Rec+ function of the host.
D001426:Bacterial Proteins; D001435:Bacteriophages / Q000235:genetics*; D004262:DNA Restriction Enzymes / Q000378:metabolism; D015245:Deoxyribonuclease BamHI; D015246:Deoxyribonuclease EcoRI; D015252:Deoxyribonucleases, Type II Site-Specific; D004352:Drug Resistance, Microbial; D005784:Gene Amplification; D010641:Phenotype; D010957:Plasmids; D011995:Recombination, Genetic; D012093:Replicon
D001426:Bacterial Proteins; D004262:DNA Restriction Enzymes; D015245:Deoxyribonuclease BamHI; D015246:Deoxyribonuclease EcoRI; C024404:BglII endonuclease; D015252:Deoxyribonucleases, Type II Site-Specific