a Department of Microbiology, Michael Reese Hospital and Medical Center, and Department of Medicine, Pritzker School of Medicine, University of Chicago, Chicago, Illinois 60616
ABSTRACT
Methicillin (intrinsic) resistance of Staphylococcus aureus was suppressed almost completely by regulatory gene (penI1) mutations of penicillinase plasmids that made penicillinase production strictly noninducible. Methicillin resistance was restored by secondary regulatory gene mutations that altered the noninducible phenotype or by complementation with a compatible plasmid that did not bear the noninducible mutation. No evidence was obtained for genetic linkage between a penicillinase plasmid and the gene for methicillin resistance. We suggest, therefore, that the mutant noninducible repressor acted in trans by binding to a site on the methicillin resistance determinant. This hypothesis would imply an appreciable degree of homology between penicillinase plasmids and methicillin resistance genes.
1 A preliminary report was presented at the 72nd Annual Meeting of American Society for Microbiology, 23-28 April 1972, Philadelphia, Pa. (Abstracts, p. 165).
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