1887

Abstract

Each of the genes in the -type cytochrome biogenesis gene cluster , plus the two flanking genes ORF117 and , were individually disrupted by Ω insertion. Resultant phenotypes were restored to the wild-type by complementation from a set of plasmids. All of the genes, but neither ORF117 nor , were required for -type cytochrome biogenesis; only was also implicated in the biosynthesis of cytochrome . Disruption of or resulted in failure to grow on rich media, but disruption of , or did not. The mutant, but not the , or mutants, also exhibited the increased sensitivity to growth inhibition by oxidized thiol compounds previously observed for the mutant. In contrast to the mutant, however, growth of the mutant on rich media could not be restored by DTT. Siderophore biosynthesis and/or secretion by was also attenuated by disruption of and but not of , or . These results indicate that CcmC can function independently of CcmA, CcmB and CcmD despite other evidence that these gene products form an ATP-binding cassette (ABC)-type-transporter with the subunit composition (CcmA)-CcmB-CcmC or (CcmA)-CcmB-CcmC-CcmD, and also suggest a possible link between the functions of CcmC and CcmG.

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1999-11-01
2024-04-18
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