In order to study the induction of terminal oxidases in Paracoccus denitrif
icans, their promoters were fused to the lacZ reporter gene and analysed in
the wild-type strain, in an FnrP-negative mutant, in a cytochrome bc(1)-ne
gative mutant, and in six single or double oxidase-negative mutant strains.
The strains were grown under aerobic, semi-aerobic, and denitrifying condi
tions. The oxygen-sensing transcriptional-regulatory protein FnrP negativel
y regulated the activity of the qox promoter, which controls expression of
the ba(3)-type quinol oxidase, while it positively regulated the activity o
f the cco promoter, which controls expression of the cbb(3)-type cytochrome
c oxidase. The ctaDII and ctaC promoters, which control the expression of
the aa(3)-type cytochrome c oxidase subunits I and II, respectively, were n
ot regulated by FnrP. The activities of the latter two promoters, however,
did decrease with decreasing oxygen concentrations in the growth medium, su
ggesting that an additional oxygen-sensing mechanism exists that regulates
transcription of ctaDII and ctaC. Apparently, the intracellular oxygen conc
entration (as sensed by FnrP) was not the only signal to which the oxidase
promoters responded. At given extracellular oxygen status, both the got and
the cco promoters responded to mutations in terminal oxidase genes, wherea
s the ctaDII and ctaC promoters did not. The change of electron distributio
n through the respiratory network, resulting from elimination of one or mor
e oxidase genes, may have changed intracellular signals that affect the act
ivities 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.