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Replication mutants of Staphylococcus aureus macrolide‐lincosamide‐streptogramin B resistance plasmid pT48
Author(s) -
Catchpole I.,
Dyke K. G. H.
Publication year - 1991
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1991.tb00771.x
Subject(s) - biology , plasmid , mutant , pentapeptide repeat , genetics , phenotype , microbiology and biotechnology , nucleic acid sequence , transposable element , lincosamides , tylosin , dna , gene , bacteria , staphylococcus aureus , biochemistry , antibiotics , peptide
Summary Copy‐number mutants of Staphylococcus aureus macrolide‐lincosamide‐streptogramin B (MLS) resistance plasmid pT48 were isolated by their resistance to the non‐inducing macrolide, tylosin. One mutant plasmid, pcopD3, showed a three‐ to five‐fold cis ‐dominant increase in copy number, and nucleotide sequence analysis revealed that the mutant had a single base change within the replication region. All other pT48 mutants examined had the unusual pheno‐type of increased plasmid multimerization and elevated copy number. These mutants were effective in trans and DNA sequencing showed that plasmids with this phenotype were deleted in one of two ways. The deletions caused similar alterations to the C ‐ter‐minus of the wild‐type pT48 Rep protein. The two types of mutant Rep proteins terminate with the same pentapeptide sequence: Ala‐Asn‐Glu‐lle‐Asp. The multimerization phenotype of these mutants can be explained by defective termination of rolling‐circle type replication.