Please use this identifier to cite or link to this item: https://doi.org/10.1186/1471-2164-6-115
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dc.titleMicroarray analysis of Pseudomonas aeruginosa reveals induction of pyocin genes in response to hydrogen peroxide
dc.contributor.authorChang, W
dc.contributor.authorSmall, D.A
dc.contributor.authorToghrol, F
dc.contributor.authorBentley, W.E
dc.date.accessioned2020-10-20T04:52:41Z
dc.date.available2020-10-20T04:52:41Z
dc.date.issued2005
dc.identifier.citationChang, 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
dc.identifier.issn14712164
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/178029
dc.description.abstractBackground: 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectantioxidant
dc.subjectcatalase
dc.subjecthydrogen peroxide
dc.subjectiron
dc.subjectprotein
dc.subjectpyocin
dc.subjectpyocin S2 immunity protein
dc.subjecttranscriptome
dc.subjectunclassified drug
dc.subjectadaptation
dc.subjectantioxidant activity
dc.subjectarticle
dc.subjectbacterial gene
dc.subjectcell metabolism
dc.subjectcystic fibrosis
dc.subjectDNA microarray
dc.subjectDNA repair
dc.subjectgene induction
dc.subjecthost pathogen interaction
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectPseudomonas aeruginosa
dc.subjectPseudomonas aeruginosa
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1186/1471-2164-6-115
dc.description.sourcetitleBMC Genomics
dc.description.volume6
dc.description.page115
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