Genetic Analysis of the γ-Aminobutyrate Utilization Pathway in Escherichia coli K-12

The control mutation that results in a concomitant severalfold increase in the activities of gamma-aminobutyrate-alpha-ketoglutarate transaminase (GSST, EC 2.6.1.19) and succinic semialdehyde dehydrogenase (SSDH, EC 1.2.1.16), leading to the acquisition of the ability to utilize gamma-aminobutyrate (GABA) as the sole source of nitrogen by Escherichia coli K-12 mutants, was mapped by mating and transduction with P1kc. The locus affected, gabC, is approximately 48% co-transduced with the thyA gene, located at min 55 of the E. coli K-12 chromosome. The structural gene of the first enzyme in the GABA pathway, GSST, was mapped by interrupted mating, using one of the GSST-less mutants, DB742, isolated in this work. The mutated locus, gabT, is situated at about min 73 of the E. coli chromosome, close to the gltC gene. Genetic evidence concerning the sensitivity of the enzymes of the GABA pathway to catabolite repression under different physiological conditions suggests that the two structural genes of the GABA regulon do not constitute one operon.