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Amino acid uptake by the general amino acid permease (Aap) of Rhizobium leguminosarum strain 3841 was greatly reduced by the presence of aspartate in the growth medium when glucose was the carbon source. This was due to the prevention of uptake and not by transcriptional repression. However, the Ntr-regulated gene glnII was repressed by aspartate. The negative regulatory effect on both the Aap and glnII was prevented by mutation of any component of the dicarboxylate transport system or by the inclusion of a C4-dicarboxylate in the growth medium, including the non-metabolizable analogue 2-methylsuccinate.

Enzyme assays suggest the involvement of 2-keto-myo-inositol and D-2,3-diketo-4-deoxy epi-inositol in the myo-inositol catabolism of Rhizobium leguminosarum bv. viciae. Growth of R. leguminosarum on myo-inositol increases the enzyme's myo-inositol dehydrogenase and 2-keto-myo-inositol dehydratase. Examination of the growth in glucose as carbon source and resuspension studies in myo-inositol show that O2 consumption is an inducible route. Mutation studies reveal the necessity of intra-cellular dicarboxylation for the repression of these enzymes. Isolation and studies of three transposon mutants that do not induce both enzymes suggest that myo-inositol is not vital as an energy source in bacteriods.

A Tn5 mutant (RU301) of R. leguminosarum that lacks the O-antigen, and which has rough colony morphology and is unable to swarm in TY agar, produces only lipopolysaccharide layer (LPS II). RU301 fails to grow on organic acids but high concentration of calcium or magnesium restores the growth. Southern blotting shows the location at transposon insertion in RU301 in a 3 kb EcoRI fragment. There is a separation of 10 kb between dctD and the region mutated in strain RU301. Additional calcium is not necessary for all LPS rough mutants, and gene mutation in RU301 is essential for nitrogen fixation.