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Microarray analysis of Pseudomonas aeruginosa reveals induction of pyocin genes in response to hydrogen peroxide

Authors
Publisher
BioMed Central
Publication Date
Source
PMC
Keywords
  • Research Article
Disciplines
  • Biology

Abstract

1471-2164-6-115.fm ral ss BioMed CentBMC Genomics Open AcceResearch article Microarray analysis of Pseudomonas aeruginosa reveals induction of pyocin genes in response to hydrogen peroxide Wook Chang1, David A Small1, Freshteh Toghrol*2 and William E Bentley1 Address: 1Center for Biosystems Research, University of Maryland Biotechnology Institute, College Park, Maryland 20742, USA and 2Microarray Research Laboratory, Biological and Economic Analysis Division, Office of Pesticide Programs, U. S. Environmental Protection Agency, Fort Meade, Maryland 20755, USA Email: Wook Chang - [email protected]; David A Small - [email protected]; Freshteh Toghrol* - [email protected]; William E Bentley - [email protected] * Corresponding author 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 oxidat

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