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Transcriptomic analysis of acquired resistance to a novel trimethoprim-based photoswitchable antibiotic in Escherichia coli CS1562

ABSTRACT: Transcriptomic analysis of acquired resistance to a novel trimethoprim-based photoswitchable antibiotic in Escherichia coli CS1562

PROVIDER: PRJNA715103 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13987585_1.fastq.gz	Fastqsanger.gz
	SRR13987585_2.fastq.gz	Fastqsanger.gz
	SRR13987586_1.fastq.gz	Fastqsanger.gz
	SRR13987586_2.fastq.gz	Fastqsanger.gz
	SRR13987587_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of acquired resistance to a novel trimethoprim-based photoswitchable antibiotic in Escherichia coli CS1562

Project description:Effect of three different antimicrobial compounds, trimethoprim(TMP), cis-tetra-ortho-chloroazobenzene-trimethoprim (TCATa) and trans-tetra-ortho-chloroazobenzene-trimethoprim (TCATd) , on the resistance development and transcriptome of the E. coli strain CS1562. In addition, acontrol sample was taken along of the propagated parent strain (CS1562) without the addition of any compounds.

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Pyrrole-based inhibitors of RND-type efflux pumps reverse antibiotic resistance and display antivirulence potential

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Transcription profiling by array of Burkholderia cenocepacia antibiotic adapted resistant mutants after antibiotic stress

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A novel antibiotic resistance mechanism

Project description:A novel antibiotic resistance mechanism

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

Project description: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.

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Gene expression profiling of trimethoprim resistant Escherichia coli

Project description:Global alterations in trimethoprim (TMP) resistant E. coli are unknown. TMP resistant E. coli have been developed in the laboratory over a period of 48 hours by step-wise increase in TMP concentration and gene expression profiles have been obtained to identify genome wide perturbations in trimethoprim resistance. Biological duplicates of wild-type E. coli MG1655, E. coli resistant to 2 ug/ ml TMP (4xR) and E. coli resistant to 16 ug/ml TMP (32xR) were analyzed.

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Project description:The antibiotic trimethoprim (TMP) is used to treat a variety of Escherichia coli infections, but its efficacy is limited by the rapid emergence of TMP-resistant bacteria. Previous laboratory evolution experiments have identified resistance-conferring mutations in the gene encoding the TMP target, bacterial dihydrofolate reductase (DHFR), in particular mutation L28R. Here, we show that 4'-desmethyltrimethoprim (4'-DTMP) inhibits both DHFR and its L28R variant, and selects against the emergence of TMP-resistant bacteria that carry the L28R mutation in laboratory experiments. Furthermore, antibiotic-sensitive E. coli populations acquire antibiotic resistance at a substantially slower rate when grown in the presence of 4'-DTMP than in the presence of TMP. We find that 4'-DTMP impedes evolution of resistance by selecting against resistant genotypes with the L28R mutation and diverting genetic trajectories to other resistance-conferring DHFR mutations with catalytic deficiencies. Our results demonstrate how a detailed characterization of resistance-conferring mutations in a target enzyme can help identify potential drugs against antibiotic-resistant bacteria, which may ultimately increase long-term efficacy of antimicrobial therapies by modulating evolutionary trajectories that lead to resistance.

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Detection of antibiotic resistance genes in human gut microbiota

Project description:We used a DNA microarray chip covering 369 resistance types to investigate the relation of antibiotic resistance gene diversity with humansM-bM-^@M-^Y age. Metagenomic DNA from fecal samples of 123 healthy volunteers of four different age groups, i.e. pre-school Children (CH), School Children (SC), High School Students (HSS) and Adults (AD) were used for hybridization. The results showed that 80 different gene types were recovered from the 123 individuals gut microbiota, among which 25 were present in CH, 37 in SC, 58 in HSS and 72 in AD. Further analysis indicated that antibiotic resistance genes in groups of CH, SC and AD can be independently clustered, and those ones in group HSS are more divergent. The detailed analysis of antibiotic resistance genes in human gut is further described in the paper DNA microarray analysis reveals the antibiotic resistance gene diversity in human gut microbiota is age-related submitted to Sentific Reports The antibiotic resistance gene microarray is custom-designed (Roche NimbleGen), based on a single chip containing 3 internal replicated probe sets of 12 probes per resistance gene, covering the whole 315K 12-plex platform spots.

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