Distinctive Oxidative Stress Responses to Hydrogen Peroxide in Sulfate Reducing Bacteria Desulfovibrio vulgaris Hildenborough

Journal Article · Thu Jan 01 04:00:00 EST 2009 · TBD

OSTI ID:973374

Zhou, Aifen; He, Zhili; Redding, A M; Mukhopadhyay, Aindrila; Hemme, Christopher L; Joachimiak, Marcin P; Bender, Kelly S; Keasling, Jay D; Stahl, David A; Fields, Matthew W; Hazen, Terry C; Arkin, Adam P; Wall, Judy D; Zhou, Jizhong

Response of Desulfovibrio vulgaris Hildenborough to hydrogen peroxide (H2O2, 1 mM) was investigated with transcriptomic, proteomic and genetic approaches. Microarray data demonstrated that gene expression was extensively affected by H2O2 with the response peaking at 120 min after H2O2 treatment. Genes affected include those involved with energy production, sulfate reduction, ribosomal structure and translation, H2O2 scavenging, posttranslational modification and DNA repair as evidenced by gene coexpression networks generated via a random matrix-theory based approach. Data from this study support the hypothesis that both PerR and Fur play important roles in H2O2-induced oxidative stress response. First, both PerR and Fur regulon genes were significantly up-regulated. Second, predicted PerR regulon genes ahpC and rbr2 were derepressedin Delta PerR and Delta Fur mutants and induction of neither gene was observed in both Delta PerR and Delta Fur when challenged with peroxide, suggesting possible overlap of these regulons. Third, both Delta PerR and Delta Fur appeared to be more tolerant of H2O2 as measured by optical density. Forth, proteomics data suggested de-repression of Fur during the oxidative stress response. In terms of the intracellular enzymatic H2O2 scavenging, gene expression data suggested that Rdl and Rbr2 may play major roles in the detoxification of H2O2. In addition, induction of thioredoxin reductase and thioredoxin appeared to be independent of PerR and Fur. Considering all data together, D. vulgaris employed a distinctive stress resistance mechanism to defend against increased cellular H2O2, and the temporal gene expression changes were consistent with the slowdown of cell growth at the onset of oxidative stress.

• Research Organization: Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, CA (US)
• Sponsoring Organization: Earth Sciences Division; Genomics Division; Physical Biosciences Division
• DOE Contract Number: AC02-05CH11231
• OSTI ID: 973374
• Report Number(s): LBNL-2535E
• Journal Information: TBD, Journal Name: TBD
• Country of Publication: United States
• Language: English

Related Subjects

59 BASIC BIOLOGICAL SCIENCES
DESULFOVIBRIO
DETOXIFICATION
DNA REPAIR
GENES
GENETICS
HYDROGEN PEROXIDE
HYPOTHESIS
INDUCTION
MODIFICATIONS
MUTANTS
OPACITY
OXIDOREDUCTASES
PRODUCTION
Response of Desulfovibrio vulgaris Hildenborough
distinctive stress resistance mechanism
slowdown of cell growth
onset of oxidative stress
SCAVENGING
SULFATE-REDUCING BACTERIA
SULFATES