Duncan C L, Strong D H, Sebald M
J Bacteriol. 1972 Apr;110(1):378-91. doi: 10.1128/jb.110.1.378-391.1972.
The ability of Clostridium perfringens type A to produce an enterotoxin active in human food poisoning has been shown to be directly related to the ability of the organism to sporulate. Enterotoxin was produced only in a sporulation medium and not in a growth medium in which sporulation was repressed. Mutants with an altered ability to sporulate were isolated from an sp(+) ent(+) strain either as spontaneous mutants or after mutagenesis with acridine orange or nitrosoguanidine. All sp(0) (-) mutants were ent(-). Except for one isolate, these mutants were not disturbed in other toxic functions characteristic of the wild type and unrelated to sporulation. A total of four of seven osp(0) mutants retained the ability to produce detectable levels of enterotoxin. None of the ent(-) mutants produced gene products serologically homologous to enterotoxin. A total of three sp(-) mutants, blocked at intermediate stages of sporulation, produced enterotoxin. Of these mutants, one was blocked at stage III, one probably at late stage IV, and one probably at stage V. A total of three sp(+) revertants isolated from an sp(-) ent(-) mutant regained not only the ability to sporulate but also the ability to produce enterotoxin. The enterotoxin appears to be a sporulation-specific gene product; however, the function of the enterotoxin in sporulation is unknown.
A型产气荚膜梭菌产生对人类食物中毒具有活性的肠毒素的能力已被证明与该生物体形成芽孢的能力直接相关。肠毒素仅在芽孢形成培养基中产生，而不在抑制芽孢形成的生长培养基中产生。从sp(+) ent(+)菌株中分离出芽孢形成能力改变的突变体，这些突变体要么是自发突变体，要么是经吖啶橙或亚硝基胍诱变后获得的。所有sp(0) (-)突变体均为ent(-)。除了一个分离株外，这些突变体在野生型的其他与芽孢形成无关的毒性功能方面未受干扰。七个osp(0)突变体中有四个仍保留产生可检测水平肠毒素的能力。没有一个ent(-)突变体产生与肠毒素血清学同源的基因产物。共有三个在芽孢形成中间阶段受阻的sp(-)突变体产生了肠毒素。在这些突变体中，一个在III期受阻，一个可能在IV期末受阻，一个可能在V期受阻。从一个sp(-) ent(-)突变体中分离出的三个sp(+)回复突变体不仅恢复了形成芽孢的能力，还恢复了产生肠毒素的能力。肠毒素似乎是一种芽孢形成特异性基因产物；然而，肠毒素在芽孢形成中的功能尚不清楚。
