Kanei C, Uchida T, Yoneda M
Infect Immun. 1977 Oct;18(1):203-9. doi: 10.1128/iai.18.1.203-209.1977.
Five mutants that produce toxin in medium with excess iron were isolated from strain C7(beta). The iron content of bacteria grown on this medium was considerably higher than that of C7(beta) cells grown in medium containing the minimum amount of iron needed to inhibit toxin production. When the nonlysogenic, nontoxinogenic strain C7(-) was lysogenized with phages from each of the mutants, toxin production by all of the resulting lysogens, like that by parent strain C7(beta), ceased upon iron addition. When the mutants were superinfected with beta45 phage, both toxin and CRM45 were produced in medium with excess iron. One of the mutant strains lost its prophage as a result of treatment with ultraviolet light. When the cured strain was lysogenized with phage carrying a mutation in the tox structural gene, the lysogen produced the mutant protein at the maximum rate in medium with excess iron. These findings show that the mutant strains are not phage mutants, but are bacterial host mutants, and that a host factor(s) is involved in the inhibition of toxin production by iron.
从菌株C7(β)中分离出了五个在铁过量的培养基中产生毒素的突变体。在此培养基上生长的细菌的铁含量明显高于在含有抑制毒素产生所需最低铁量的培养基中生长的C7(β)细胞。当非溶原性、不产毒素的菌株C7(-)被来自每个突变体的噬菌体溶原化时,所有产生的溶原菌产生毒素的情况,与亲代菌株C7(β)一样,在添加铁后停止。当突变体被β45噬菌体超感染时,在铁过量的培养基中会产生毒素和CRM45。其中一个突变菌株因紫外线处理而失去了原噬菌体。当用携带tox结构基因突变的噬菌体使治愈的菌株溶原化时,该溶原菌在铁过量的培养基中以最大速率产生突变蛋白。这些发现表明,突变菌株不是噬菌体突变体,而是细菌宿主突变体,并且一种宿主因子参与了铁对毒素产生的抑制作用。