Forsgren A, Nordström K, Philipson L, Sjöquist J
J Bacteriol. 1971 Jul;107(1):245-50. doi: 10.1128/jb.107.1.245-250.1971.
Staphylococcus aureus Cowan I was exposed to nitrosoguanidine or ethyl-methanesulfonate, and survivors were screened on nutrient agar plates containing rabbit anti-protein A serum for loss of protein A production. More than half of all protein A-deficient mutants also lacked nuclease, coagulase, alpha hemolysin, fibrinolysin, mannitol utilization, and the phage-type pattern. Mutants with a spectrum of these properties were also isolated. Induced or spontaneous reversions of the mutants were observed. The properties of the protein A-deficient mutants suggest that synthesis or release (or both) of a number of extracellular products of S. aureus is controlled by a common regulatory mechanism.
金黄色葡萄球菌考恩I株暴露于亚硝基胍或甲基磺酸乙酯,在含有兔抗蛋白A血清的营养琼脂平板上筛选存活菌株,以检测蛋白A产生的缺失情况。超过一半的蛋白A缺陷型突变体还缺乏核酸酶、凝固酶、α溶血素、纤维蛋白溶解酶、甘露醇利用能力以及噬菌体类型模式。还分离出具有一系列这些特性的突变体。观察到了突变体的诱导或自发回复突变。蛋白A缺陷型突变体的特性表明,金黄色葡萄球菌许多细胞外产物的合成或释放(或两者)受一种共同调节机制的控制。