Transcriptional Organization and Regulation of the l -Idonic Acid Pathway (GntII System) in Escherichia coli

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Abstract
The genetic organization of the idn genes that encode the pathway for l -idonate catabolism was characterized. The monocistronic idnK gene is transcribed divergently from the idnDOTR genes, which were shown to form an operon. The 215-bp regulatory region between the idnK and idnD genes contains promoters in opposite orientation with transcription start sites that mapped to positions −26 and −29 with respect to the start codons. The regulatory region also contains a single putative IdnR/GntR binding site centered between the two promoters, a CRP binding site upstream of idnD , and an UP element upstream of idnK . The genes of the l -idonate pathway were shown to be under catabolite repression control. Analysis of idnD - and idnK - lacZ fusions in a nonpolar idnD mutant that is unable to interconvert l -idonate and 5-ketogluconate indicated that either compound could induce the pathway. The l -idonate pathway was first characterized as a subsidiary pathway for d -gluconate catabolism (GntII), which is induced by d -gluconate in a GntI (primary gluconate system) mutant. Here we showed that the idnK and idnD operons are induced by d -gluconate in a GntI system mutant, presumably by endogenous formation of 5-ketogluconate from d -gluconate. Thus, the regulation of the GntII system is appropriate for this pathway, which is primarily involved in l -idonate catabolism; the GntII system can be induced by d -gluconate under conditions that block the GntI system.