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Two‐pronged survival strategy for the major cystic fibrosis pathogen, Pseudomonas aeruginosa , lacking the capacity to degrade nitric oxide during anaerobic respiration
Author(s) -
Yoon Sang Sun,
Karabulut Ahmet C,
Lipscomb John D,
Hennigan Robert F,
Lymar Sergei V,
Groce Stephanie L,
Herr Andrew B,
Howell Michael L,
Kiley Patricia J,
Schurr Michael J,
Gaston Benjamin,
Choi KyoungHee,
Schweizer Herbert P,
Hassett Daniel J
Publication year - 2007
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601787
Subject(s) - library science , biology , gerontology , medicine , computer science
Protection from NO gas, a toxic byproduct of anaerobic respiration in Pseudomonas aeruginosa , is mediated by nitric oxide (NO) reductase (NOR), the norCB gene product. Nevertheless, a norCB mutant that accumulated ∼13.6 μM NO paradoxically survived anaerobic growth. Transcription of genes encoding nitrate and nitrite reductases, the enzymes responsible for NO production, was reduced >50‐ and 2.5‐fold in the norCB mutant. This was due, in part, to a predicted compromise of the [4Fe–4S] 2+ cluster in the anaerobic regulator ANR by physiological NO levels, resulting in an inability to bind to its cognate promoter DNA sequences. Remarkably, two O 2 ‐dependent dioxygenases, h o m o g entisate‐1,2‐dioxygenase (HmgA) and 4‐ h ydroxyphenyl p yruvate d ioxygenase (Hpd), were derepressed in the norCB mutant. Electron paramagnetic resonance studies showed that HmgA and Hpd bound NO avidly, and helped protect the norCB mutant in anaerobic biofilms. These data suggest that protection of a P. aeruginosa norCB mutant against anaerobic NO toxicity occurs by both control of NO supply and reassignment of metabolic enzymes to the task of NO sequestration.