Iron uptake in colicin B-resistant mutants of Escherichia coli K-12

Abstract

Four classes of colicin B-resistant mutants of Escherichia coli K-12 were examined for defects in iron uptake. All four mutant classes (cbt, exbC, exbB, and tonB) were defective in the uptake of ferri-enterochelin. The tonB mutant was also defective in citrate-, ferrichrome-, and rhodoturulic acid-mediated iron uptake. The defects in iron transport were reflected in increased sensitivity to iron chelators and to chromium and aluminium salts, and in hypersecretion of enterochelin. One of the mutants (cbt) was apparently defective in outer membrane ferri-enterochelin receptor activity. aroE derivatives (unable to synthesize enterochelin) of the four mutant classes and the parent strain produced increased amounts of two outer membrane polypeptides when grown under iron stress. These polypeptides are implicated in ferri-enterochelin receptor activity.

The importance of the exbB gene for vitamin B12 and ferric iron transport

“…Previously characterized exbB mutants produced 250-fold more enterochelin than the wild-type, indicating that their iron metabolism was disturbed [12]. It was subsequently shown that exbB mutants are partly deficient in ferric enterochelin uptake [13] although in contrast to our observation the mutant studied was normal in ferrichrome uptake. Our method for isolating the mutants by transposon insertion may have destroyed the function, or exerted a strong polar effect on several genes in the exbB gene region.…”

“…In exbB strains the plating efficiency for T1 is normal; the plating of T5 is inhibited by ferrichrome in tonB strains [16]-this was not observed with exbB mutants (data not shown); the transport of iron via enterochelin, citrate and dihydroxybenzoate can occur in exbB mutants although less efficiently than in the parent strain. This may be the reason why the exbB strain excreted 250-fold and the tonB strain 1000-fold more enterochelin than the parent strain [13]. All this data including the regulation of exbB by iron indicates that, like tonB, exbB is involved in ferric iron and vitamin B 12 uptake mediated by outer membrane receptors.…”

“…Another property of the exbB mutants is their tolerance to the B group colicins, B, D, G, H, Ia, Ib, M, S1 and V [4,13]. The exbB strains able to produce enterochelin are tolerant to higher doses of colicin than exbB strains which cannot make enterochelin [4,9].…”

The Phenotypic and Fitness Effects of Colicin Resistance in Escherichia coli K-12

“…As has been detailed previously, there are additional beneficial consequences of colicin resistance, including resistance to multiple colicins and phage resistance (Hancock et al 1976). There are also possible additional deleterious effects of resistance, beyond the growth rate differences in rich media reported here, such as reduced nutrient uptake (Pugsley and Reeves 1976) and increased sensitivity to antibiotics, bile salts, and detergents (Savage 1977;Mitsuoka 1996).…”

“…Thus, it is predicted that high levels of resistance should be costly to maintain unless there is continuous exposure to colicins. Receptor-based resistance in some cases can lower growth rates when certain nutrients are limiting (Pugsley and Reeves 1976); tolerance can also disrupt the integrity of the cell membrane, making the cell more susceptible to environmental perturbations (Webster 1991). However, no experiment has been specifically designed to assess the fitness effects of colicin resistance.…”