SUMMARY: Mutants isolated from strain PAO1632 (HutAmi) were unable to utilize -arginine or -ornithine as the carbon source for growth. Arginine deiminase (AD), catabolic ornithine carbamoyltransferase (cOTC) and -acetylornithine 5-aminotrans-ferase (ACOAT) were present in the mutants but these enzymes were not induced to higher levels by exogenous -arginine. One group of mutants could utilize -ornithine but not -arginine and in these strains -arginine induced the synthesis of ACOAT but not AD or cOTC. The mutations of the arginine utilization-negative mutants were all in genes of the same transductional linkage group and mapped in the 45 to 50 min region of the chromosome. Revertants isolated on -arginine or -ornithine plates were derepressed for the synthesis of ACOAT. It is suggested that -arginine is normally catabolized by the wild-type strain via the arginine deiminase pathway and requires a threshold level of ACOAT. The regulatory factors controlling the functioning of the divergent arginine deiminase and arginine carboxylase pathways are discussed.


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