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首页> 外文期刊>Journal of bacteriology >Modulation of Protein A Formation in Staphylococcus aureus by Genetic Determinants for Methicillin Resistance
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Modulation of Protein A Formation in Staphylococcus aureus by Genetic Determinants for Methicillin Resistance

机译：甲氧西林耐药性遗传决定因素对金黄色葡萄球菌蛋白A形成的调控

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Many methicillin-resistant (Mecr) strains of Staphylococcus aureus either produce no protein A or secrete it extracellularly (S. Winblad and C. Ericson, Acta Pathol. Microbiol. Scand. Sect. B >81:150–156, 1973). We found that methicillin resistance and protein A production were apparently lost coordinately from the natively Mecr strain A676. Restoration of the genetic determinant for methicillin resistance (mec) by transduction or transformation restored protein A production. In two other Mecr strains, loss of mec was accompanied by marked reduction in protein A formation. Genetic transfer of mec to derivatives of S. aureus 8325 affected protein A formation differently with different mec determinants. Those derived from strain A676 and two other Mecr strains reduced the scanty amount of protein A produced by strain 8325 to even lower or undetectable levels, whereas mec from two more Mecr strains increased its protein A content. This “mec-effect,” i.e., stimulation or inhibition of protein A formation dependent on the combination of host strain and mec determinant, was reduced in methicillin-susceptible (Mecs) mutants produced by ethyl methane sulfonate treatment of Mecr strains. The mec-effect reappeared in spontaneous revertants to methicillin resistance. Phenotypic reduction of methicillin resistance in Mecr strains grown at 44°C was accompanied by reduction of the mec-effect on protein A, but it had no effect on protein A formation in Mecs strains. Two independent mutants of strain 8325 produced large amounts of protein A at rates that were unaffected by growth at 44°C or by the introduction of mec determinants.
机译：许多金黄色葡萄球菌的耐甲氧西林（Mec r ）菌株不产生蛋白A或不分泌蛋白A（S. Winblad和C.Ericson，Acta Pathol.Microbiol.Scand B > 81： 150-156，1973年）。我们发现，甲氧西林抗性和蛋白A的产生显然是由Mec r 天然菌株A676协调丧失的。通过转导或转化来恢复甲氧西林抗性的遗传决定因子（ mec ）恢复了蛋白A的产生。在另外两个Mec r 菌株中， mec 的丧失伴随着蛋白A形成的明显减少。 mec 遗传转化为 S的衍生物。不同的 mec 决定因素对金黄色葡萄球菌8325的影响不同。那些来自菌株A676和其他两个Mec r 菌株的蛋白将8325菌株产生的蛋白A的稀少程度降低到甚至更低或不可检测的水平，而 mec 则来自另外两个Mec < sup> r 菌株增加了其蛋白A含量。这种“ mec 效应”，即刺激或抑制依赖宿主菌株和 mec 决定簇的蛋白A的形成，在甲氧西林敏感性（Mec <甲烷磺酸乙酯处理Mec r 菌株产生的sup> s ）突变体。 mec 效应在自发回复株对甲氧西林的耐药性中再次出现。表型降低在44°C生长的Mec r 菌株中甲氧西林的耐药性，同时降低 mec 对蛋白A的作用，但对蛋白A的形成没有影响在Mec s 菌株中。两个菌株8325的两个独立突变体以不受44°C生长或引入 mec 决定簇影响的速率产生了大量的蛋白A。

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