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Deletion of BmoR affects the expression of genes related to thiol/disulfide balance in Bacteroides fragilis

dc.contributor.authorTeixeira, Felipe L.
dc.contributor.authorPauer, Heidi
dc.contributor.authorCosta, Scarlathe B.
dc.contributor.authorSmith, C. Jeffrey
dc.contributor.authorDomingues, Regina M. C. P.
dc.contributor.authorRocha, Edson R.
dc.contributor.authorLobo, Leandro A.
dc.date.accessioned2020-05-05T16:25:33Z
dc.date.available2020-05-05T16:25:33Z
dc.date.issued2018-09-26
dc.description.abstractBacteroides fragilis, an opportunistic pathogen and commensal bacterium in the gut, is one the most aerotolerant species among strict anaerobes. However, the mechanisms that control gene regulation in response to oxidative stress are not completely understood. In this study, we show that the MarR type regulator, BmoR, regulates the expression of genes involved in the homeostasis of intracellular redox state. Transcriptome analysis showed that absence of BmoR leads to altered expression in total of 167 genes. Sixteen of these genes had a 2-fold or greater change in their expression. Most of these genes are related to LPS biosynthesis and carbohydrates metabolism, but there was a signifcant increase in the expression of genes related to the redox balance inside the cell. A pyridine nucleotide-disulfde oxidoreductase located directly upstream of bmoR was shown to be repressed by direct binding of BmoR to the promoter region. The expression of two other genes, coding for a thiosulphate:quinoneoxidoreductase and a thioredoxin, are indirectly afected by bmoR mutation during oxygen exposure. Phenotypic assays showed that BmoR is important to maintain the thiol/disulfde balance in the cell, confrming its relevance to B. fragilis response to oxidative stress.en_US
dc.identifier.doi10.1038/s41598-018-32880-7
dc.identifier.urihttp://hdl.handle.net/10342/8495
dc.titleDeletion of BmoR affects the expression of genes related to thiol/disulfide balance in Bacteroides fragilisen_US
dc.typeArticleen_US
ecu.journal.nameScientific Reportsen_US
ecu.journal.pages14405en_US
ecu.journal.volume8en_US

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