Cohen S, Gibson C J, Sweeney H M
J Bacteriol. 1972 Nov;112(2):682-9. doi: 10.1128/jb.112.2.682-689.1972.
Methicillin (intrinsic) resistance of Staphylococcus aureus was suppressed almost completely by regulatory gene (penI(1)) 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.
青霉素酶质粒的调节基因（penI(1)）突变几乎完全抑制了金黄色葡萄球菌的甲氧西林（固有）耐药性，这些突变使青霉素酶的产生严格不可诱导。通过改变不可诱导表型的二次调节基因突变或通过与不携带不可诱导突变的相容质粒互补，甲氧西林耐药性得以恢复。未获得青霉素酶质粒与甲氧西林耐药基因之间存在遗传连锁的证据。因此，我们认为突变的不可诱导阻遏物通过与甲氧西林耐药决定簇上的一个位点结合而发挥反式作用。这一假设意味着青霉素酶质粒与甲氧西林耐药基因之间存在相当程度的同源性。
