1887

Abstract

, a causative agent of chronic hepatitis and hepatocellular carcinoma in mice, possesses a hydrogenase and a urease, both of which are nickel-containing enzymes. Analysis of the genome sequence of revealed a full set of accessory genes which are required for the nickel maturation of each enzyme in other micro-organisms. Erythromycin-resistant mutants were constructed in four of these genes, , , and . Controls for polar effect were provided for or mutants by disrupting each gene located immediately downstream, i.e. or , respectively. Urease and hydrogenase activities were determined for each strain with or without supplemented nickel in the medium. As expected, the and the mutants had negligible urease activity, but they retained normal levels of hydrogenase activity. Urease levels could not be increased by the addition of nickel to the medium. The and strains were deficient in both urease and hydrogenase activities, suggesting that both gene products act in a similar fashion as their counterparts in . However, in contrast with the analogous mutants of , the addition of nickel into the growth medium failed to restore either urease or hydrogenase enzyme levels in the or mutants, indicating a probably unique role for these genes in the mouse liver pathogen.

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2007-11-01
2024-04-19
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