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ABSTRACT: Aeromonas veronii hfq mutant transcriptome

PROVIDER: PRJNA599560 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR10849314_1.fastq.gz	Fastqsanger.gz
	SRR10849314_2.fastq.gz	Fastqsanger.gz
	SRR10849315_1.fastq.gz	Fastqsanger.gz
	SRR10849315_2.fastq.gz	Fastqsanger.gz
	SRR10849316_1.fastq.gz	Fastqsanger.gz

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Project description:To elucidate the target genes of ArgR in Aeromonas veronii, we engineered an Aeromonas veronii strain that expresses the ArgR protein fused to a 3× FLAG tag, and FLAG antibodies were employed for the immunoprecipitation of DNA-protein complexes.

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Hfq Regulates Efflux Pump Expression and Purine Metabolic Pathway to Increase the Trimethoprim Resistance in Aeromonas veronii

Project description:<p>Aeromonas veronii (A. veronii) is a zoonotic pathogen. It causes clinically a variety of diseases such as dysentery, bacteremia, and meningitis. And it also brings huge losses to aquaculture. A. veronii has been documented as a multiple antibiotic resistant bacterium. Hfq (host factor for RNA bacteriophage Qβ replication) plays vital regulation roles in a variety of cell programs. The deletion of hfq in A. veronii showed an increased sensitivity to the trimethoprim, accompanying by the down regulation of the efflux pump related genes acrA and acrB in transcriptomic data. Coherently, the complementation of acrA and acrB in ∆hfq recovered the trimethoprim resistance. Besides, the productions of adenosine and guanosine were revealed to augment in ∆hfq in metabonomic data. Both wild type and ∆hfq conferred more sensitive to trimethoprim after appending 1 mM adenosine or guanosine to M9 medium. These results demonstrated that Hfq mediated trimethoprim resistance by elevating efflux pump expression and degrading adenosine, and guanosine metabolites. Collectively, Hfq is a potential target to tackle trimethoprim resistance in A. veronii infection.</p>

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Project description:The bacterium Aeromonas veronii is a co-pathogenic species that can negatively impact the health of both humans and aquatic animals. In this study, we used single-cell transcriptome analysis (scRNA-seq) to investigate the effects of infection with A. veronii on head kidney cells and the regulation of gene expression in the dark sleeper (Odontobutis potamophila). scRNA-seq was used to assess the effects of infection with A. veronii in O. potamophila B cells, endothelial cells, macrophages, and granulocytes, and differential enrichment analysis of gene expression in B cells and granulocytes was performed. The analyses revealed a significant increase in neutrophils and decrease in eosinophils in granulocytes infected with A. veronii. Activation of neutrophils enhanced ribosome biogenesis by up-regulating the expression of rps12 and rpl12 to fight against invading pathogens. Crucial pro-inflammatory mediators il1b, ighv1-4, and the major histocompatibility class II genes mhc2a and mhc2dab, which are involved in virulence processes, were up-regulated, suggesting that A. veronii activates an immune response that presents antigens and activates immunoglobulin receptors in B cells. These cellular immune responses triggered by infection with A. veronii enriched the available scRNA-seq data for teleosts, and these results are important for understanding the evolution of cellular immune defense and functional differentiation of head kidney cells.

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MetaboLights MTBLS1411 - GNPS Hfq Regulates Efflux Pump Expression and Purine Metabolic Pathway to Increase the Trimethoprim Resistance in Aeromonas veronii

Project description:<p>Aeromonas veronii (A. veronii) is a zoonotic pathogen. It causes clinically a variety of diseases such as dysentery, bacteremia, and meningitis. And it also brings huge losses to aquaculture. A. veronii has been documented as a multiple antibiotic resistant bacterium. Hfq (host factor for RNA bacteriophage Q? replication) plays vital regulation roles in a variety of cell programs. The deletion of hfq in A. veronii showed an increased sensitivity to the trimethoprim, accompanying by the down regulation of the efflux pump related genes acrA and acrB in transcriptomic data. Coherently, the complementation of acrA and acrB in ?hfq recovered the trimethoprim resistance. Besides, the productions of adenosine and guanosine were revealed to augment in ?hfq in metabonomic data. Both wild type and ?hfq conferred more sensitive to trimethoprim after appending 1 mM adenosine or guanosine to M9 medium. These results demonstrated that Hfq mediated trimethoprim resistance by elevating efflux pump expression and degrading adenosine, and guanosine metabolites. Collectively, Hfq is a potential target to tackle trimethoprim resistance in A. veronii infection.</p>

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