Identification of the OsbR regulon in Chromobacterium violaceum
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PROVIDER: PRJNA721207 | ENA |
REPOSITORIES: ENA
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Project description:Here, we described a novel transcriptional regulator belonging to the MarR family that we named OsbR (oxidative stress response and biofilm formation regulator) in the opportunistic pathogen Chromobacterium violaceum. Transcriptome profiling by DNA microarray using strains with deletion or overexpression of osbR showed that OsbR exert a global regulatory role in C. violaceum, regulating genes involved in oxidative stress response, nitrate reduction, biofilm formation, and several metabolic pathways. EMSA assays showed that OsbR binds to the promoter regions of several OsbR-regulated genes and the in vitro DNA binding activity was inhibited by oxidants. We demonstrated that the overexpression of osbR caused activation of ohrA even in the presence of the repressor OhrR, which resulted in improved growth under organic hydroperoxide treatment. We showed that the proper regulation of the nar genes by OsbR ensures an optimal growth of C. violaceum under anaerobic conditions by tuning the reduction of nitrate to nitrite. Finally, the osbR overexpressing strain showed reduction in biofilm formation and this phenotype correlated with the OsbR-mediated repression of two gene clusters encoding putative adhesins.
2021-04-11 | GSE171860 | GEO
Project description:Identification of the EmrR regulon in Chromobacterium violaceum
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Project description:Antibiotic resistance can arise by several mechanisms, including mutation in transcription factors that regulate drug efflux pumps. In this work, we identified EmrR as a MarR family transcription factor involved in antibiotic resistance in Chromobacterium violaceum, a Gram-negative bacterium that occurs in soil and water and can act as a human opportunistic pathogen. Antibiogram and minimum inhibitory concentration (MIC) assays showed that the ΔemrR mutant presented increased resistance to the antibiotic nalidixic acid in respect to the wild-type strain. The emrR gene is near to a putative operon emrCAB, which encode the efflux pump EmrCAB. DNA Microarray analysis showed that EmrR represses the emrCAB operon and some other putative transporters. Northern blot assays validated that EmrR represses the emrCAB operon and this repression can be released by salicylate, but not other compounds such as nalidixic acid or ethidium bromide. Electrophoretic mobility shift assays (EMSA) showed that EmrR binds directly to the promoter regions of emrR, emrCAB and other genes to exert negative regulation. Therefore, in response to compounds as salicylate, EmrR derepresses the operon emrCAB causing overexpression of the efflux pump EmrCAB and increased resistance to nalidixic acid in C. violaceum.
2018-11-01 | GSE112521 | GEO
Project description:Histone-like nucleoid structuring (H-NS) proteins silence horizontally-acquired genes, facilitating their the acquisition and integration of important traits such as virulence and antibiotic resistance in bacterial pathogens. In this work, we describe the H-NS proteins in the environmental opportunistic pathogen Chromobacterium violaceum. We show that C. violaceum encodes two H-NS proteins, Chn1 and Chn2. Transcriptomic analyses revealed that Chn1 is the predominant H-NS-family protein in C. violaceum, repressing many genes, while Chn2 is largely compensatory, exhibiting a phenotype only in a double mutant, chn1 chn2 strain. This is reinforced by in silico analyses showing that chn1 is conserved throughout Chromobacterium, while chn2 is species-dependent, and likely horizontally-acquired. The expression of 213 genes, including the Chromobacterium pathogenic island 2 (Cpi-2), was de-repressed in the chn1 chn2 mutant. Phenotypic analyses revealed altered virulence, violacein production, motility and acid and osmolarity tolerance in chn1 and chn1 chn2 mutant strains, demonstrating the prominent role of these H-NS-family proteins as global regulators of virulence-associated traits in C. violaceum.
2026-08-31 | GSE304743 | GEO
Project description:In this study, we used transcriptional profiling to define the adaptive response of C. violaceum to oxidative stress induced by cumene hydroperoxide (CHP) and to identify the OhrR regulon. DNA microarray and northern blot analysis revealed that in CHP-treated cells occur strong upregulation of genes involved in many pathways for stress protection, including antioxidant enzymes (catalase and peroxidases), thioredoxin, glutaredoxin and lipoyl-dependent reducing systems, DNA repair enzymes, heat shock response (σ32 regulon), iron limitation (Fur regulon) and nitrogen starvation. Genes encoding glyoxalases, glutathione S-transferases and oxygenases were also induced, suggesting further catabolism of the aromatic compound CHP. Pathways downregulated by CHP stress include electron transport chain, nucleotide biosynthesis and unsaturation of fatty acids. Further, we identified two upregulated genes (OhrA and a protein with GGDEF domain for c-di-GMP synthesis) and three downregulated genes (hemolysin, chitinase and collagenase) in the ohrR mutant. Using a mouse infection model, we demonstrate that the ohrR mutant, but not the ohrA mutant, is attenuated for virulence and showed a decreased bacterial burden in the liver. Therefore, we have defined the CHP stimulon and determined that C. violaceum uses the organic hydroperoxide sensor OhrR for regulate expression of genes required to antioxidant defense and to modulate virulence in its interaction with the host.
2017-05-01 | GSE90551 | GEO
Project description:Cumene hydroperoxide stimulon and OhrR regulon in Chromobacterium violaceum
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Project description:Bacteria in polymicrobial communities engage in complex interactions, including interbacterial antagonism. In Chromobacterium violaceum, the Type VI Secretion System (T6SS) serves as a critical antibacterial weapon, but the full set of effectors delivered by this system remains not yet completely defined. To comprehensively identify T6SS effectors, we performed co-immunoprecipitation of VgrG3, one of the six VgrGs encoded by C. violaceum, followed by LC–MS/MS analysis. Comparative proteomics revealed a diverse array of VgrG3-associated proteins, including all six VgrG homologs, phospholipase effectors from the Tle1 and Tle5 families, PAAR-domain proteins, Tap-1–like adaptors, and the Rhs-family protein RhsF. Functional analyses confirmed that RhsF acts as a T6SS-dependent antibacterial toxin neutralized by its cognate immunity protein, RhsFi (CV_1430), forming a toxin-immunity pair. X-ray crystallography of the RhsF-CT/RhsFi complex at 1.85 Å resolution revealed structural features of ADP-ribosyltransferases in RhsF and demonstrated that RhsFi inhibits toxicity by directly occluding the catalytic site. Mutagenesis assays further confirmed that RhsF toxicity depends on a catalytic triad composed of residues R1403, Y1456, and E1497. These findings expand the known repertoire of T6SS toxins in C. violaceum and place RhsF as a newly identified antibacterial effector in this bacterium.
2026-08-24 | PXD071369 | Pride
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