EFFECTS OF NITRATE RESPIRATION ON EXPRESSION OF THE ARC-CONTROLLED OPERONS ENCODING SUCCINATE-DEHYDROGENASE AND FLAVIN-LINKED L-LACTATE DEHYDROGENASE

Expression of sdhCDAB (encoding succinate dehydrogenase) and lctD (enc oding the flavin-linked L-lactate dehydrogenase) is elevated aerobical ly and repressed anaerobically in Escherichia coli. The repression is initiated by autophosphorylation of the sensor protein ArcB, followed by phosphoryl group transfer to the regulator ArcA. ArcA-P, a global t ranscriptional regulator, then prevents sdh and lct expression. The st imulus for ArcB is not O-2 deficiency per se. In vitro experiments sho wed that ArcB phosphorylation is enhanced by pyruvate, D-lactate, acet ate, and NADH, the concentrations of which are likely to increase with the lack of an effective exogenous electron sink. In addition to thei r aerobic function, the two primary dehydrogenases also have roles in anaerobic nitrate respiration. Results presented here indicate that th e increase of sdh and lct expression by nitrate depended on its chemic al reduction, which in turn diminished the ArcA-P pool. Unexpectedly, a mutation in the fnr gene (encoding a global regulator involved in an aerobic metabolism) also alleviated the anaerobic repressions. Mutatio ns in arcB or arcA were epistatic over that of fnr. Moreover, since th is relief was counteracted by pyruvate in the growth medium, Fnr appea rs to affect formation of stimuli for ArcB. It is possible that Fnr al so indirectly affects some of the other members of the arcA modulon, e .g., cyoABCDE (encoding the cytochrome o complex), cydAB (encoding the cytochrome d complex), and sodA (encoding the manganese-dependent sup eroxide dismutase).