A discrete role for FNR in the transcriptional response to moderate changes in oxygen by Haemophilus influenzae Rd KW20.
The survival by pathogenic bacteria within the specific conditions of an anatomical niche is critical for their persistence. These conditions include the combination of toxic chemicals, such as reactive oxygen (ROS) and reactive nitrogen species (RNS), with factors relevant to cell growth, such as oxygen. Haemophilus influenzae senses oxygen levels largely through the redox state of the intracellular fumarate-nitrate global regulator (FNR). H. influenzae certainly encounters oxygen levels that fluctuate, but in reality, these would rarely reach a state that results in FNR being fully reduced or oxidized. We were therefore interested in the response of H. influenzae to ROS and RNS at moderately high or low oxygen levels and the corresponding role of FNR. At these levels of oxygen, even though the growth rate of an H. influenzae fnr mutant was similar to wild type, its ROS and RNS tolerance was significantly different. Additionally, the subtle changes in oxygen did alter the whole cell transcriptional profile and this was different between the wild type and fnr mutant strains. It was the changed whole cell profile that impacted on ROS/RNS defence, but surprisingly, the FNR-regulated, anaerobic nitrite reductase (NrfA) continued to be expressed and had a role in this phenotype.
Research Centre for Infectious Disease, The University of Adelaide, Adelaide, Australia; School of Biological Science, The University of Adelaide, Adelaide, Australia; Agri-Food and Veterinary Authority of Singapore, Singapore. Electronic address: Donald_JIANG@ava.gov.sg.
Donald
D
Jiang
Research Centre for Infectious Disease, The University of Adelaide, Adelaide, Australia; School of Biological Science, The University of Adelaide, Adelaide, Australia. Electronic address: alexandra.tikhomirova@adelaide.edu.au.
Alexandra
A
Tikhomirova
School of Biological Science, The University of Adelaide, Adelaide, Australia; Robinson Research Institute, The University of Adelaide, Adelaide, Australia. Electronic address: Stephen.bent@adelaide.edu.au.
Stephen J
SJ
Bent
Research Centre for Infectious Disease, The University of Adelaide, Adelaide, Australia; School of Biological Science, The University of Adelaide, Adelaide, Australia. Electronic address: stephen.kidd@adelaide.edu.au.
Stephen P
SP
Kidd
D000332:Aerobiosis; D000693:Anaerobiosis; D015964:Gene Expression Regulation, Bacterial; D006193:Haemophilus influenzae / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D026361:Reactive Nitrogen Species / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000633:toxicity*; D012264:Ribonucleotide Reductases / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism*; D014158:Transcription, Genetic
D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D014157:Transcription Factors; D012264:Ribonucleotide Reductases; C101141:anaerobic ribonucleotide reductase; D010100:Oxygen
Aerobic/anaerobic; FNR; Haemophilus influenza; Oxidative stress