Please use this identifier to cite or link to this item: https://doi.org/10.1186/1471-2164-6-115
Title: Microarray analysis of Pseudomonas aeruginosa reveals induction of pyocin genes in response to hydrogen peroxide
Authors: Chang, W 
Small, D.A
Toghrol, F
Bentley, W.E
Keywords: antioxidant
catalase
hydrogen peroxide
iron
protein
pyocin
pyocin S2 immunity protein
transcriptome
unclassified drug
adaptation
antioxidant activity
article
bacterial gene
cell metabolism
cystic fibrosis
DNA microarray
DNA repair
gene induction
host pathogen interaction
nonhuman
oxidative stress
Pseudomonas aeruginosa
Pseudomonas aeruginosa
Issue Date: 2005
Citation: Chang, W, Small, D.A, Toghrol, F, Bentley, W.E (2005). Microarray analysis of Pseudomonas aeruginosa reveals induction of pyocin genes in response to hydrogen peroxide. BMC Genomics 6 : 115. ScholarBank@NUS Repository. https://doi.org/10.1186/1471-2164-6-115
Rights: Attribution 4.0 International
Abstract: Background: Pseudomonas aeruginosa, a pathogen infecting those with cystic fibrosis, encounters toxicity from phagocyte-derived reactive oxidants including hydrogen peroxide during active infection. P. aeruginosa responds with adaptive and protective strategies against these toxic species to effectively infect humans. Despite advances in our understanding of the responses to oxidative stress in many specific cases, the connectivity between targeted protective genes and the rest of cell metabolism remains obscure. Results: Herein, we performed a genome-wide transcriptome analysis of the cellular responses to hydrogen peroxide in order to determine a more complete picture of how oxidative stress-induced genes are related and regulated. Our data reinforce the previous conclusion that DNA repair proteins and catalases may be among the most vital antioxidant defense systems of P. aeruginosa. Our results also suggest that sublethal oxidative damage reduces active and/or facilitated transport and that intracellular iron might be a key factor for a relationship between oxidative stress and iron regulation. Perhaps most intriguingly, we revealed that the transcription of all F-, R-, and S-type pyocins was upregulated by oxidative stress and at the same time, a cell immunity protein (pyocin S2 immunity protein) was downregulated, possibly leading to self-killing activity. Conclusions: This finding proposes that pyocin production might be another novel defensive scheme against oxidative attack by host cells. © 2005 Chang et al., licensee BioMed Central Ltd.
Source Title: BMC Genomics
URI: https://scholarbank.nus.edu.sg/handle/10635/178029
ISSN: 14712164
DOI: 10.1186/1471-2164-6-115
Rights: Attribution 4.0 International
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