Active Transport of beta-Galactosides by a Mutant of Escherichia coli Defective in Heme Synthesis

Abstract

1 A mutant of Escherichia coli strain ML308-225 defective in 5-aminolevulinic acid synthesis has been isolated. When grown in the absence of this supplement the cytochrome content of the cells is less than 0.1% compared to the wild type. 2 When supplemented with 5-aminolevulinic acid the transport of β-galactoside by cells of the mutant are comparable to that of the wild type, i.e. transport is inhibited 40% by both the respiratory inhibitor cyanide or the ATPase inhibitor dicyclohexylcarbodiimide. In contrast, however, when the mutant is grown without 5-aminolevulinic acid the transport by cells is not inhibited by cyanide but is reduced by about 80% with dicyclohexylcarbodiimide. 3 Membrane vesicles prepared from cells grown without 5-aminolevulinic acid show no d-lactate-dependent transport of lactose. 4 The experiments are in accordance with the current idea, that either respiration or ATP-hydrolysis can supply energy for the active transport of β-galactosides.