Loss of the oxidative stress regulator OxyR in Pseudomonas aeruginosa PAO1 impairs growth under iron limited conditions

Pyoverdine is the main siderophore secreted by fluorescent pseudomonads to
scavenge iron in the extracellular environment. Iron uptake, however, needs to be
tightly regulated, because free iron stimulates the formation of highly toxic oxygen
derivatives. In the opportunistic pathogen Pseudomonas aeruginosa, the transcriptional
regulator OxyR plays a key role in the upregulation of defense mechanisms
against oxidative stress as it stimulates the expression of the antioxidant genes
katB, ahpB and ahpCF after contact with oxidative stress-generating agents.
Inactivation of the oxyR gene in Pseudomonas fluorescens ATCC 17400 and in
P. aeruginosa PAO1 impairs pyoverdine-mediated iron uptake. The pyoverdine
utilization defect can be restored by complementation with the oxyR gene of
P. aeruginosa, as well as by adding catalase. Growth of the oxyR mutant in low- or
high-iron media is also impaired at a low, but not at a high inoculum density.
Uptake of radioactive 59Fe pyoverdine is, however, not affected by the oxyR
mutation, nor is the transcription of the fpvA gene encoding the ferripyoverdine
receptor, suggesting that the defect lies in the inability to remove iron from the
ferrisiderophore.

Jaar van publicatie:2008

Trefwoorden:Pseudomonas, siderophore, OxyR