Identification of the Bacteroides fragilis EcfO regulon 3
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ABSTRACT: Genome expression study of Bacteroides fragilis strain 638R comparing a EcfO/anti-EcfO null mutant with an empty vector to a EcfO/anti-EcfO null mutant containing the EcfO gene on a plasmid under the control of a maltose inducible promoter.
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing a EcfO/anti-EcfO null mutant with an empty vector to a EcfO/anti-EcfO null mutant containing the EcfO gene on a plasmid under the control of a maltose inducible promoter. Two chip study with 8 technical replicates on each chip comparing the EcfO overexpressing strain in a EcfO/anti-EcfO mutant to an empty vector control in the same mutant background.
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing a EcfO null mutant with an empty vector to a anti-EcfO null mutant containing the EcfO gene on a plasmid under the control of an IPTG inducible promoter.
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing an ecfO null mutant with an empty vector to a reo (anti-ecfO) null mutant containing the ecfO gene on a plasmid under the control of an IPTG inducible promoter.
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing a EcfO null mutant with an empty vector to a anti-EcfO null mutant containing the EcfO gene on a plasmid under the control of an IPTG inducible promoter. Two chip study with 8 technical replicates on each chip comparing the EcfO overexpressing strain in an anti-EcfO mutant to an empty vector control in a EcfO null mutant.
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing an ecfO null mutant with an empty vector to a reo (anti-ecfO) null mutant containing the ecfO gene on a plasmid under the control of an IPTG inducible promoter. Seven chip study with 8 technical replicates (i.e. Each probe replicated 8 times on the chip) on each chip comparing the ecfO overexpressing strain in a reo (anti-ecfO) mutant to an empty vector control in an ecfO null mutant.
Project description:Genome expression study of Bacteroides fragilis ATCC25285 strain containing the EcfO gene constitutively expressed from plasmid pFD340
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing a fur deletion mutant with the wild-type strain grown in minimal defined media with iron-replete or iron-limiting conditions following oxygen exposure. The construction of the fur mutant analyzed in this study was described in Robertson KP, Smith CJ, Gough AM, Rocha ER. Characterization of Bacteroides fragilis hemolysins and regulation and synergistic interactions of HlyA and HlyB. Infect Immun. 2006 74:2304-2316.
Project description:Genome expression study of Bacteroides fragilis strain 638R comparing an fur deletion mutant with the wild-type strain grown in minimal defined media with iron-replete, iron-limiting, heme-replete and heme-limiting conditions. The construction of the fur mutant analyzed in this study was described in Robertson KP, Smith CJ, Gough AM, Rocha ER. Characterization of Bacteroides fragilis hemolysins and regulation and synergistic interactions of HlyA and HlyB. Infect Immun. 2006 74:2304-2316.
Project description:Genome expression study of Bacteroides fragilis ATCC25285 strain containing the EcfO gene constitutively expressed from plasmid pFD340 Two chip study with 5 technical replicates on each chip comparing the EcfO overexpressing strain to an empty vector control in the wild type strain.
Project description:Bacteroides fragilis is an anaerobic commensal in the human gut which can act as opportunistic pathogen when leaving its intestinal niche to reach other body sites. Bacteroides infections have a high lethality and must be treated by antimicrobial chemotherapy. Metronidazole is one of the most frequently administered antimicrobials in the treatment of Bacteroides infections and is highly reliable. However, metronidazole resistance does occur, favoring fatal disease outcomes. Most of the resistant isolates harbor a nim gene (12 are currently known, i.e. nimA to nimL), a transferable resistance determinant for metronidazole. Previous research suggested that Nim proteins might affect the cellular physiology by changing the activity of key enzymes like pyruvate:ferredoxin oxidoreductase (PFOR). In this study we wanted to assess the impact of the nimA gene on protein expression in a standard B. fragilis isolate, 638R, and compared overall protein expression in 638R with and without a nim gene and with the nimA gene in a proteomic study. Further, high-level metronidazole resistance was induced in both strains and the protein expression profiles of resulting resistant daughter strains were also compared with their respective parent strains. We found that comparably few proteins displayed altered expression in 638R with the nimA gene, but flavodiiron protein FprA was repeatedly found upregulated. FprA is often found in anaerobes and reduces molecular oxygen to water and/or nitric oxide to nitrous oxide. After induction of metronidazole resistance, a far higher number of proteins were found to be differentially expressed in 638R without nimA than in 638R with nimA. In the former, factors for the import of hemin were strongly downregulated, indicating impaired iron import, whereas in the latter the observed changes were not only less numerous but also less specific. Based on the results of this study we present a novel hypothetic model of metronidazole resistance and Nim function.