An mutant of was constructed by replacing the chromosomal gene by an internally deleted derivative containing a cassette. Southern and Western blotting confirmed that the gene had been replaced by the disrupted gene and that the aconitase A protein was no longer expressed. However, the mutant failed to exhibit the anticipated glutamate auxotrophy and it retained a residual aconitase activity. This activity was due to an analogous unstable enzyme(s) designated aconitase B. Studies on the regulation of aconitase A synthesis using an translational fusion showed that the gene resembles other citric acid cycle genes in being subject to CRP-mediated catabolite repression and ArcA-mediated anaerobic repression. In addition to being activated by the SoxRS oxidative stress regulatory system, the gene appeared to be activated by the ferric uptake regulator (Fur). It was concluded that the gene belongs to at least four global regulatory networks, and In contrast, the aconitase B activity decreased after exposure to oxidative stress and was less affected by anaerobiosis. Comparable studies with the fumarase genes ( and ) indicated that (encoding the unstable aerobic iron-sulphur-containing fumarase) is by the ferric uptake regulator (Fur) and (encoding the stable fumarase) is activated by the SoxRS oxidative stress regulatory system.


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