
Regulation of expression of terminal oxidases in Paracoccus denitrificans
Author(s) -
Otten Marijke F.,
Stork David M.,
Reijnders Willem N. M.,
Westerhoff Hans V.,
Van Spanning Rob J. M.
Publication year - 2001
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1046/j.1432-1327.2001.02131.x
Subject(s) - paracoccus denitrificans , promoter , cytochrome c oxidase , mutant , oxidase test , biology , microbiology and biotechnology , biochemistry , cytochrome , chemistry , gene expression , gene , enzyme
In order to study the induction of terminal oxidases in Paracoccus denitrificans , their promoters were fused to the lac Z reporter gene and analysed in the wild‐type strain, in an FnrP‐negative mutant, in a cytochrome bc 1 ‐negative mutant, and in six single or double oxidase‐negative mutant strains. The strains were grown under aerobic, semi‐aerobic, and denitrifying conditions. The oxygen‐sensing transcriptional‐regulatory protein FnrP negatively regulated the activity of the qox promoter, which controls expression of the ba 3 ‐type quinol oxidase, while it positively regulated the activity of the cco promoter, which controls expression of the cbb 3 ‐type cytochrome c oxidase. The cta DII and cta C promoters, which control the expression of the aa 3 ‐type cytochrome c oxidase subunits I and II, respectively, were not regulated by FnrP. The activities of the latter two promoters, however, did decrease with decreasing oxygen concentrations in the growth medium, suggesting that an additional oxygen‐sensing mechanism exists that regulates transcription of cta DII and cta C. Apparently, the intracellular oxygen concentration (as sensed by FnrP) was not the only signal to which the oxidase promoters responded. At given extracellular oxygen status, both the qox and the cco promoters responded to mutations in terminal oxidase genes, whereas the cta DII and cta C promoters did not. The change of electron distribution through the respiratory network, resulting from elimination of one or more oxidase genes, may have changed intracellular signals that affect the activities of the qox and cco promoters. On the other hand, the re‐routing of electron distribution in the respiratory mutants hardly affected the oxygen consumption rate as compared to that of the wild‐type. This suggests that the mutants adapted their respiratory network in such a way that they were able to consume oxygen at a rate similar to that of the wild‐type strain.