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pubmed-article:8231803pubmed:abstractTextThe incompatibility that pSC101-derived plasmids express toward each other is mediated by directly repeated sequences (iterons) located near the plasmid's replication origin. We report here that the pSC101 par locus, which stabilizes plasmid inheritance in dividing cell populations and alters DNA superhelicity, can function as a cis-acting enhancer of incompatibility, which we show is determined jointly by the copy number of the plasmid and the number of iterons per copy. A single synthetic 32 bp iteron sequence carried by the pUC19 plasmid confers strong pSC101-specific incompatibility in the absence of any other pSC101 sites but requires the par locus to express strong incompatibility when carried by a lower-copy-number plasmid. We propose a model by which the par locus can enhance the apparently antagonistic processes of incompatibility and pSC101 DNA replication while concurrently facilitating plasmid distribution during cell division.lld:pubmed
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pubmed-article:8231803pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:8231803pubmed:articleTitleThe partition (par) locus of pSC101 is an enhancer of plasmid incompatibility.lld:pubmed
pubmed-article:8231803pubmed:affiliationDepartment of Genetics, Stanford University School of Medicine, California 94305.lld:pubmed
pubmed-article:8231803pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8231803pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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