Genetic instability of M protein and serum opacity factor of group A streptocci: evidence suggesting extrachromosomal control
Genetic instability of M protein and serum opacity factor of group A streptocci: evidence suggesting extrachromosomal control
复制标题
A 组链球菌 M 蛋白和血清混浊因子的遗传不稳定性：提示染色体外控制的证据
作者：
P. Cleary;Z. Johnson;L. Wannamaker
M抗原是A组链球菌毒力的主要决定因素，在生物学上表现为对吞噬作用的抗性，已知在体内和体外都会发生各种表型变化。这些变化是非随机的，可能发生的频率很高。使用先前描述的血清混浊反应（与某些菌株相关）与M抗原存在之间的关系，分析M抗原的表型不稳定性。结果支持了M蛋白合成和血清混浊反应直接或间接受同一基因控制或受连锁分离的基因控制的结论。此外，生长条件和固化剂利福平和溴化乙锭的分离克隆不能表现出血清混浊因子和抵抗吞噬人类白细胞有明显的影响。连续转移四株A组链球菌的静止期培养物显着增加了血清混浊反应和M抗原阴性的菌落数。对于四个菌株中的两个，溴化乙锭和利福平也增加了具有这种表型的菌落的分离。根据这些实验和必要的控制，质粒或噬菌体在调节M蛋白合成的可能影响进行了讨论。
The M antigen, a primary determinant of virulence in group A streptococci that is expressed biologically as resistance to phagocytosis, is known to undergo a variety of phenotypic changes both in vivo and in vitro. These changes are nonrandom and can occur at a high frequency. Using the previously described relationship between the serum opacity reaction (associated with certain strains) and the presence of the M antigen, the phenotypic instability of the M antigen was analyzed. The results support the conclusion that M protein synthesis and the serum opacity reaction are directly or indirectly controlled by the same gene or by genes which are linked and can segregate as a unit. Moreover, growth conditions and the curing agents rifampin and ethidium bromide had a discernible influence on the segregation of clones unable to exhibit serum opacity factor and to resist phagocytosis by human leukocytes. Serial transfer of stationary-phase cultures of four strains of group A streptococci significantly increased the number of colonies negative for the serum opacity reaction and the M antigen. For two of four strains both ethidium bromide and rifampin also increased the segregation of colonies with this phenotype. In light of these experiments and the necessary controls, the possible influence of plasmids or bacteriophage in regulating M protein synthesis is discussed.