The nac gene of Klebsiella aerogenes.

Abstract

In enteric bacteria, transcription of a large family of genes is regulated by the Nitrogen Regulatory (Ntr) System in response to the availability of nitrogen. The isolation of insertion mutations in a gene called nac demonstrates that control of several nitrogen-regulated genes by the Ntr System is mediated indirectly. K. aerogenes cells containing null mutations in nac are unable to activate expression of hut (histidine utilization), put (proline utilization), and ure (urea utilization), or to repress formation of gdh (glutamate dehydrogenase), and gltB (glutamate synthase). These nac null mutants are still able to regulate expression of glnA (glutamine synthetase), nar (nitrate reductase) and nif (nitrogen fixation), and are unaffected in the regulation of the Ntr System itself. Studies of K. aerogenes nac mutants in which the E. coli lacZ gene is under control of the nac promoter indicate that expression of nac is regulated by the availability of nitrogen and by the Ntr System. A DNA fragment of approximately 13 kb containing the K. aerogenes nac gene was cloned. Complementation studies performed using the cloned nac gene and several independently derived nac insertion mutants suggest that nac modulates its own expression and that the nac locus encodes at least two functions: one involved in the regulation of nac target operons, the other involved in the regulation of nac itself. Wild-type Salmonella typhimurium cells strongly resemble K. aerogenes nac mutants. In wild-type S. typhimurium, operons such as glnA, which are regulated directly by the Ntr System, are activated in response to nitrogen limitation, but operons such as hut, which are indirectly regulated by Ntr control, are not. Introduction of a plasmid containing the K. aerogenes nac gene into S. typhimurium allows S. typhimurium to activate hut expression during nitrogen-limited growth. Thus, nac is either missing or defective in S. typhimurium.