Genetic and Metabolic Control of Histidase and Urocanase in Salmonella typhimurium, Strain 15–59

Salmonella typhimurium strain 15–59 can use l-histidine as a source of nitrogen, except when glucose is the major source of carbon. Upon induction by histidine the organism produces histidase and urocanase. The formation of these enzymes is strongly repressed by glucose. A series of mutants, either deficient in the ability to metabolize histidine or altered in the control of the formation of the histidine-degrading enzymes, was isolated. It could be shown that the genetic sites for control (constitutive formation of the enzymes, or resistance to repression by glucose, or inability to form both histidase and urocanase) are closely linked to the sites where mutation results in the specific inability to produce either histidase or urocanase. The mutation to constitutivity affects not only histidase and urocanase, but also another enzyme required for the degradation of histidine, formiminoglutamate hydrolase; mutation to resistance to repression by glucose affects only histidase and urocanase. The actual inducer appears to be urocanic acid and not histidine. However, urocanic acid cannot be used for induction since it fails to penetrate the cell. There is coordinate control of the synthesis of histidase and urocanase; the close linkage of the genes responsible for the formation of these enzymes suggests that they belong to a single operon.