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Next Generation Sequencing of Wildtype and Thioredoxin-A knockout of a clinical isolate of Acinetobacter baumannii

ABSTRACT: Next Generation Sequencing of Wildtype and Thioredoxin-A knockout of a clinical isolate of Acinetobacter baumannii

PROVIDER: PRJNA514926 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8438371.fastq.gz	Fastqsanger.gz
	SRR8438372.fastq.gz	Fastqsanger.gz
	SRR8438373.fastq.gz	Fastqsanger.gz
	SRR8438374.fastq.gz	Fastqsanger.gz
	SRR8438375.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing of Wildtype and Thioredoxin-A knockout of a clinical isolate of Acinetobacter baumannii

Project description:RNA sequencing was used to analyze the transcriptome of a thioredoxin-A knockout of a clinical isolate of Acinetobacter baumannii

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Project description:The bacterial pathogen, Acinetobacter baumannii, is a leading cause of drug-resistant infections. Here, we investigated the potential of developing nanobodies that specifically recognize A. baumannii over other Gram-negative bacteria. Through generation and panning of a synthetic nanobody library, we identified several potential lead candidates. We demonstrate how incorporation of next generation sequencing analysis can aid in selection of lead candidates for further characterization. Using monoclonal phage display, we validated the binding of several lead nanobodies to A. baumannii. Subsequent purification and biochemical characterization revealed one particularly robust nanobody that broadly and specifically bound A. baumannii compared to other common drug resistant pathogens. These findings support the potentially for nanobodies to selectively target A. baumannii and the identification of lead candidates for possible future diagnostic and therapeutic development.

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Shifted Metabolic Bias in Livers of Mice Lacking Hepatocytic Thioredoxin Reductase-1 Protects Against Acetaminophen Toxicity

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Project description:Genetic disruption of thioredoxin reductase 1 protects against acetaminophen (APAP) toxicity. To determine the role of the thioredoxin system on xenobiotic metabolism we challeneged wildtype and txnrd1liver-null mice with acetaminophen. Adult male wildtype and txnrd1 liver-null mice (C57BL6/J) were treated with either saline (PBS) or 100mg/kg APAP. Liver RNA was harvested eight hours after challenge and processed for microarray analysis. Comparison of 2 treatment conditions in 2 genotypes, biological replicates in triplicate.

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Transcriptional analysis of transposon mutants disrupted in glutathione biosynthesis in Acinetobacter baumannii

Project description:In this study we compare logrithmically grown Acinetobacter baumannii wildtype to a transposon mutant that is disrupted in gshA, the first step in glutathione biosynthesis using RNASeq to identify novel pathways where glutathione may be involved.

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Project description:Purpose: The goal of this study was to elucidate the collateral effects associated with OXA-23 overexpression on the Acinetobacter baumannii global transcriptome. Results: Besides the 99.73-fold increase in blaOXA-23 transcript upon IPTG induction, no other transcripts showed more than a 2-fold change compared to the wildtype control. This suggests that OXA-23 over expression to levels similarly observed in multi drug resistant A. baumannii clinical isolates does not effect the transcriptome.

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Project description:The long-term resistance to desiccation on abiotic surfaces is a key determinant of the adaptive success of Acinetobacter baumannii as a healthcare-associated bacterial pathogen. Here, the cellular and molecular mechanisms enabling A. baumannii to resist desiccation and persist on abiotic surfaces were investigated. Experiments were set up to mimic the A. baumannii response to air-drying that would occur when bacterial cells contaminate fomites in hospitals. Resistance to desiccation and transition to the “viable but nonculturable” (VBNC) state were determined in the laboratory-adapted strain ATCC 19606T and the epidemic strain ACICU. Culturability, membrane integrity, metabolic activity, virulence, and gene expression profile were compared between the two strains at different stages of desiccation. Upon desiccation, ATCC 19606T and ACICU cells lose culturability and membrane integrity, lower their metabolism, and enter the VBNC state. However, desiccated A. baumannii cells fully recover culturability and virulence in an insect infection model following rehydration in physiological buffers or human biological fluids. Transcriptome and chemical analyses of A. baumannii cells during desiccation unveiled the production of protective metabolites (L-cysteine and L-glutamate) and decreased energetic metabolism consequent to activation of the glyoxylate shunt (GS) pathway, as confirmed by reduced resuscitation efficiency of aceA mutants, lacking the key enzyme of the GS pathway. VBNC cell formation and extensive metabolic reprogramming provide a biological basis for the response of A. baumannii to desiccation, with implications on environmental control measures aimed at preventing the transmission of A. baumannii infection in hospitals.

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