Effects of fluoro-phenyl-styrene-sulfonamide (FPSS) on transcription factor sigma B regulons in Staphylococcus aureus
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PROVIDER: PRJNA1065413 | ENA |
REPOSITORIES: ENA
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Project description:Staphylococcus aureus has been shown to cause various types of tissue and systemic infections in humans and livestock with the mortality rate of 20-30%. Some isolates can be highly resistant to antibiotics hence the need to identify better drugs and drug targets. Previous studies have shown that (E)-N-(4-Fluorophenyl)-2-phenylethene sulfonamide (FPSS) could inhibit activities of a bacteria-specific transcription factor sigma B. Sigma B regulons in Bacillus subtilis and in Listeria monocytogenes, including virulence factor genes in L. monocytogenes, were decreased. Since sigma B is also presented in S. aureus, we initially postulated the use of FPSS to target S. aureus sigma B activity and to attenuate its virulence gene expression. Surprisingly, qRT-PCR results revealed that FPSS induced expression of sigma B-dependent gene asp23. RNAseq results showed 39 S. aureus genes were affected by FPSS (37 genes were downregulated and two genes were upregulated). FPSS had no effect on expression of sigB operon in S. aureus.
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2022-03-12 | E-MTAB-8703 | biostudies-arrayexpress
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2018-05-18 | GSE108967 | GEO
Project description:This data set is #3 of three generated as part of a coordinated series of experiments to examine potential modes of action of Styrene inhalation on lung and liver in male C57Bl/6 mice. Styrene causes increased lung tumors in mice, but not in rats. Mouse lung tumors were found mostly at the conclusion of a life-time (104 weeks for males) exposure study and most were benign. Styrene is largely negative in genotoxicity assays. Styrene metabolism by CYP2F2 produced a different metabolite pattern in mouse lung than in liver or in rats or humans. The purpose of this study was to use genomic analyses to further investigate potential modes of action (MoA) of styrene in mice, using a total of three genomic data sets. Dataset #1 exposed C57BL/6 wild-type (WT), CYP2F2 knockout (-/-; KO) and CYP2F21 humanized (2F2-KO + 2F1,2A13,2B6-transgenic, TG) male mice to 0, 40 or 120 ppm styrene at 6 hr/day 5 days/wk for 1 or 4 wk. Lungs were analyzed by whole genome microarrays for each strain at each dose. The second part of the study examined a broader dose response and short term exposure. Male wild type C57Bl/6 mice were exposed to 6 inhalation concentrations of styrene: 0, 1, 5, 10, 20, 40, and 120 ppm for a single 6 hour exposure. This was intended to gain dose-response data at low-observed-adverse-effect-levels (LOAELs) of styrene (≥ 20 ppm) and at no-observed-adverse-effect-levels (NOAELs) of styrene (< 20 ppm). Dataset #2 examined lung gene expression, while dataset #3 examined liver gene expression data from the same animals.
2016-11-30 | GSE75158 | GEO
Project description:This data set is #2 of three generated as part of a coordinated series of experiments to examine potential modes of action of Styrene inhalation on lung and liver in male C57Bl/6 mice. Styrene causes increased lung tumors in mice, but not in rats. Mouse lung tumors were found mostly at the conclusion of a life-time (104 weeks for males) exposure study and most were benign. Styrene is largely negative in genotoxicity assays. Styrene metabolism by CYP2F2 produced a different metabolite pattern in mouse lung than in liver or in rats or humans. The purpose of this study was to use genomic analyses to further investigate potential modes of action (MoA) of styrene in mice, using a total of three genomic data sets. Dataset #1 exposed C57BL/6 wild-type (WT), CYP2F2 knockout (-/-; KO) and CYP2F21 humanized (2F2-KO + 2F1,2A13,2B6-transgenic, TG) male mice to 0, 40 or 120 ppm styrene at 6 hr/day 5 days/wk for 1 or 4 wk. Lungs were analyzed by whole genome microarrays for each strain at each dose. The second part of the study examined a broader dose response and short term exposure. Male wild type C57Bl/6 mice were exposed to 6 inhalation concentrations of styrene: 0, 1, 5, 10, 20, 40, and 120 ppm for a single 6 hour exposure. This was intended to gain dose-response data at low-observed-adverse-effect-levels (LOAELs) of styrene (≥ 20 ppm) and at no-observed-adverse-effect-levels (NOAELs) of styrene (< 20 ppm). Dataset #2 examined lung gene expression, while dataset #3 examined liver gene expression data from the same animals.
2016-11-30 | GSE75157 | GEO
Project description:The extracytoplasmic function (ECF) σ factors are fundamental for bacterial adaptation to distinct environments and for survival under different stress conditions. The emerging pathogen Arcobacter butzleri possesses seven putative pairs of σ/anti-σ factors belonging to the ECF family. Here, we report the identification of the genes regulated by five out of the seven A. butzleri ECF σ factors. Three of the ECF σ factors play an apparent role in transport, energy generation and the maintainance of redox balance. Several genes like the nap, sox and tct genes are regulated by more than one ECF σ factor indicating that the A. butzleri ECF σ factors form a network of overlapping regulons. In contrast to other eubacteria, these A. butzleri ECF regulons appear to primarily regulate responses to changing environments in order to meet metabolic needs instead of an obvious role in stress adaptation.
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Project description:Abstract of associated manuscript: The Bacillus subtilis extracytoplasmic function (ECF) sigma(M) factor is activated by cell envelope stress elicited by antibiotics, and by acid, heat, ethanol and superoxide stresses. Here, we have used several complementary approaches to identify genes controlled by sigma(M). In many cases, expression is only partially dependent on sigma(M) because of both overlapping promoter recognition with other ECF sigma factors and the presence of additional promoter elements. Genes regulated by sigma(M) have a characteristic pattern of induction in response to cell envelope-acting antibiotics as evidenced by hierarchical clustering analysis. sigma(M) also contributes to the expression of the Spx transcription factor and thereby indirectly regulates genes of the Spx regulon. Cell envelope stress responses also include regulons controlled by sigma(W), sigma(B) and several two-component regulatory systems (e.g. LiaRS, YycFG, BceRS). Activation of the sigma(M) regulon increases expression of proteins functioning in transcriptional control, cell wall synthesis and shape determination, cell division, DNA damage monitoring, recombinational repair and detoxification.
2008-12-05 | GSE13820 | GEO
Project description:In this study, we performed a ChIP-chip experiment to determine the respective regulons of RpoHI and RpoHII in Rhodobacter sphaeroides. We grew R. sphaeroides in aerobic conditions and induced either proteins ectopically and immuno-precipitated the regions of the genomic DNA interacting with the sigma factors.
2012-08-03 | GSE39711 | GEO
Project description:Lung gene expression after long-term (26 weeks, 52 weeks, 78 weeks & 104 weeks) styrene inhalation exposure at a single concentration (120ppm) in three strains of C57BL/6 mice -- wild-type (WT), CYP2F2 knockout (KO), and CYP2F1 humanized (TG) mice, and CD-1 mice. These data examine transcriptomic changes in lung tissue after long-term styrene inhalation in male C57Bl/6 and CD-1 mice. Styrene causes increased lung tumors in mice, but not in rats. Mouse lung tumors were found mostly at the conclusion of a life-time (104 weeks for males) exposure study and most were benign. Styrene is largely negative in genotoxicity assays. Styrene metabolism by CYP2F2 produced a different metabolite pattern in mouse lung than in liver or in rats or humans. The purpose of this study was to use genomic analyses to further investigate potential modes of action (MoA) of styrene in mice after long-term exposure to styrene. Mice strains exposed were C57BL/6 wild-type (WT), CYP2F2 knockout (-/-; KO) and CYP2F21 humanized transgenic (2F2-KO + 2F1,2A13,2B6-transgenic, TG), and CD-1 male mice using 120 ppm styrene at 6 hr/day 5 days/wk for 26, 52, 78 and 104 weeks. Lungs were analyzed by Affymetrix whole genome microarrays for each strain relative to sample time-specific vehicle controls for each strain.
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