Organization of the Electron Transfer Chain to Oxygen in the Obligate Human Pathogen Neisseria gonorrhoeae: Roles for Cytochromes c4 and c5, but Not Cytochrome c2, in Oxygen Reduction


Although Neisseria gonorrhoeae is a prolific source of eight c-type cytochromes, little is known about how its electron transfer pathways to oxygen are organized. In this study, the roles in the respiratory chain to oxygen of cytochromes c2, c4, and c5, encoded by the genes cccA, cycA, and cycB, respectively, have been investigated. Single mutations in genes for either cytochrome c4 or c5 resulted in an increased sensitivity to growth inhibition by excess oxygen and small decreases in the respiratory capacity of the parent, which were complemented by the chromosomal integration of an ectopic, isopropyl--D-thiogalactopyranoside (IPTG)-inducible copy of the cycA or cycB gene. In contrast, a cccA mutant reduced oxygen slightly more rapidly than the parent, suggesting that cccA is expressed but cytochrome c2 is not involved in electron transfer to cytochrome oxidase. The deletion of cccA increased the sensitivity of the cycB mutant to excess oxygen but decreased the sensitivity of the cycA mutant. Despite many attempts, a double mutant defective in both cytochromes c4 and c5 could not be isolated. However, a strain with the ectopically encoded, IPTG-inducible cycB gene with deletions in both cycA and cycB was constructed: the growth and survival of this strain were dependent upon the addition of IPTG, so gonococcal survival is dependent upon the synthesis of either cytochrome c4 or c5. These results define the gonococcal electron transfer chain to oxygen in which cytochromes c4 and c5, but not cytochrome c2, provide alternative pathways for electron transfer from the cytochrome bc1 complex to the terminal oxidase cytochrom

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