| Abstract: | When a strain (arcB-) of Escherichia coli, unable to synthesize the iron transport compound enterochelin, was transduced to tonB-, it became resistant to phage phi80 and simultaneously lost the growth response to enterochelin and the ability to transport its iron complex. However, enterochelin precursors (shikimate and 2,3-dihydroxybenzoate) still supported growth, via the synthesis of enterochelin. Dihydroxybenzoate was a better growth factor at a low concentration than it was at higher levels. The evidence suggests that tonB- strains lack an outer membrane component necessary both for the uptake of ferric-enterochelin and for the adsorption of phage phi80. Thus, although ferric-enterochelin cannot penetrate the cell surface from outside, the complex that is formed within the envelope is transported normally into the cell. The aroB-, tonB- mutant also lacked growth reponses to citrate and various hydroxamate siderochromes, which supported growth in the tonB+ parent strain via inducible transport systems for their ferric complexes. The aroB-, tonB- mutant was unable to transport iron in the presence of citrate, but the low-affinity uptake of uncomplexed iron and the transport of amino acids and phosphate were unimpaired. The tonB locus, thus, affects all the known active transport systems for iron, possibly indicating that they share some common outer membrane component. |
