Wayne R, Frick K, Neilands J B
J Bacteriol. 1976 Apr;126(1):7-12. doi: 10.1128/jb.126.1.7-12.1976.
A variety of natural and synthetic siderophores capable of supporting the growth of Escherichia coli K-12 on iron-limited media also protect strain RW193+ (tonA+ ent-) from the killing action of colicins B, V, and Ia. Protective activity falls into two categories. The first, characteristic of enterobactin protection against colicin B and ferrichrome protection against colicin M, has properties of a specific receptor competition between the siderophore and the colicin. Thus, enterobactin specifically protects against colicin B in fes- mutants (able to accumulate but unable to utilize enterobactin) as predicted by our proposal that the colicin B receptor functions in the specific binding for uptake of enterobactin (Wayne and Neilands, 1975). Similarly ferrichrome specifically protects against colicin M in SidA mutants (defective in hydroxamate siderophore utilization). The second category of protective response, characteristic of the more general siderophore inhibition of colicins B, V, and Ia, requires the availability or metabolism of siderophore iron. Thus, enterobactin protects against colicins V and Ia, but only when the colicin indicator strain is fes+, and hydroxamate siderophores inhibit colicins B, V, and Ia, but only when the colicin indicator strain is SidA+. Moreover, ferrichrome inhibits colicins B, V, and Ia, yet chromium (III) deferriferrichrome is inactive, and ferrichrome itself does not prevent adsorption of colicin Ia receptor material in vitro. Although the nonspecific protection against colicins B, V, and Ia requires iron, the availability of siderophore iron for cell growth is not sufficient to bring about protection. None of the siderophores tested protect cells against the killing action of colicin E1 or K, or against the energy poisons azide, 2, 4-dinitrophenol, and carbonylcyanide m-chlorophenylhydrazone. We suggest that nonspecific siderophore protection against colicins B, V, and Ia may be due either to an induction of membrane alterations in response to siderophore iron metabolism or to a direct interference by siderophore iron with some unknown step in colicin action subsequent to adsorption.
多种能够在铁限制培养基上支持大肠杆菌K-12生长的天然和合成铁载体，也能保护RW193 +菌株（tonA + ent-）免受大肠菌素B、V和Ia的杀伤作用。保护活性分为两类。第一类，如肠杆菌素对大肠菌素B的保护以及铁色素对大肠菌素M的保护，具有铁载体与大肠菌素之间特异性受体竞争的特性。因此，正如我们所提出的大肠菌素B受体在肠杆菌素摄取的特异性结合中起作用（Wayne和Neilands，1975），肠杆菌素在fes-突变体（能够积累但不能利用肠杆菌素）中特异性地保护细胞免受大肠菌素B的侵害。同样，铁色素在SidA突变体（异羟肟酸铁载体利用缺陷）中特异性地保护细胞免受大肠菌素M的侵害。第二类保护反应，是更普遍的铁载体对大肠菌素B、V和Ia的抑制作用的特征，需要铁载体铁的可用性或代谢。因此，肠杆菌素能保护细胞免受大肠菌素V和Ia的侵害，但仅当大肠菌素指示菌株为fes +时；异羟肟酸铁载体能抑制大肠菌素B、V和Ia，但仅当大肠菌素指示菌株为SidA +时。此外，铁色素能抑制大肠菌素B、V和Ia，但铬（III）去铁铁色素无活性，并且铁色素本身在体外不能阻止大肠菌素Ia受体物质的吸附。尽管对大肠菌素B、V和Ia的非特异性保护需要铁，但铁载体铁对细胞生长的可用性不足以带来保护作用。所测试的任何一种铁载体都不能保护细胞免受大肠菌素E1或K的杀伤作用，也不能保护细胞免受能量毒物叠氮化物、2,4-二硝基苯酚和羰基氰化物间氯苯腙的侵害。我们认为，铁载体对大肠菌素B、V和Ia的非特异性保护可能是由于响应铁载体铁代谢而诱导的膜改变，或者是由于铁载体铁在吸附后对大肠菌素作用中某个未知步骤的直接干扰。
