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A class of Azotobacter chroococcum mutants induced by Tn1 that were defective in normal aerobic nitrogen fixation when grown on sugars (Fos-) were corrected by provision of alpha-ketoglutarate or glutamate. In a representative mutant, Fos252, rates of evolution of 14CO2 from [14C]acetate or [14C]glucose were 5% of the parental values, although uptake and incorporation were normal for both substrates. The results suggest that a lesion affects the entry of substrates into the tricarboxylic acid cycle. The activity of citrate synthase in Fos252 in vitro was 5% that of the parents. The citrate synthase (gltA) gene from Escherichia coli was cloned into broad-host-range vectors and mobilized into Fos252. The plasmids restored parental citrate synthase activities to Fos252 and complemented the inability to fix N2 in air. The data indicate that a mutation causing an intrinsic limitation in respiratory capacity abolishes normal aerobic N2 fixation, which is consistent with the hypothesis of respiratory protection for nitrogenase in Azotobacter species.

Lesions in citrate synthase that affect aerobic nitrogen fixation by Azotobacter chroococcum