Hordeum brevisubulatum subsp. violaceum
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ABSTRACT:
PROVIDER: PRJNA674667 | ENA |
REPOSITORIES: ENA
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Project description:Hordeum brevisubulatum subsp. violaceum Genome sequencing and assembly
| PRJNA672802 | ENA
Project description:Hordeum brevisubulatum subsp. brevisubulatum Genome sequencing
| PRJNA1005068 | ENA
Project description:Hordeum brevisubulatum Genome sequencing
| PRJNA612571 | ENA
Project description:Hordeum brevisubulatum Genome sequencing
| PRJNA1288173 | ENA
Project description:Hordeum brevisubulatum Transcriptome or Gene expression
| PRJNA545813 | ENA
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: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: Not available
| S-EPMC7782175 | biostudies-literature
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