Characterizing Acinetobacter baumannii desiccation tolerance.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA436809 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6801311.fastq.gz | Fastqsanger.gz | |||
| SRR6801312.fastq.gz | Fastqsanger.gz | |||
| SRR6801313.fastq.gz | Fastqsanger.gz | |||
| SRR6801314.fastq.gz | Fastqsanger.gz | |||
| SRR6801315.fastq.gz | Fastqsanger.gz |
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Project description:Desiccation tolerance has been implicated as an important characteristic that potentiates the spread of the bacterial pathogen Acinetobacter baumannii through hospitals on dry surfaces. Despite the potential importance of this stress response, scarce information is available describing the underlying mechanisms of A. baumannii desiccation tolerance. Here we characterize the factors influencing desiccation survival of A. baumannii. At the macroscale level, we find that desiccation tolerance is influenced by cell density, growth phase, and desiccation medium. Our transcriptome analysis indicates that desiccation represents a unique state for A. baumannii compared to commonly studied growth conditions and strongly influences pathways responsible for proteostasis. Remarkably, we find that an increase in total cellular protein aggregates, which is often considered deleterious, correlates positively with the ability of A. baumannii to survive desiccation. We show that artificially inducing protein aggregate formation increases desiccation survival, and more importantly, that proteins incorporated into cellular aggregates can retain activity. Our results suggest that protein aggregates may promote desiccation tolerance in A. baumannii through preserving and protecting proteins from damage during desiccation until rehydration occurs.
2018-10-27 | GSE111383 | GEO
Project description:Hospital environments serve as excellent reservoirs for the opportunistic pathogen Acinetobacter baumannii in part because it is exceptionally tolerant to desiccation. To understand the functional basis this trait, we used transposon sequencing (Tn-seq) to identify genes contributing to desiccation tolerance in A. baumannii strain AB5075. We identified 142 candidate desiccation tolerance genes, one of which encoded the global post-transcriptional regulator CsrA. We characterized CsrA in more detail by using proteomics to identify proteins that were differentially present in wild type and csrA mutant cells. Among these were a predicted universal stress protein A, an iron-containing redox protein, a KGG-domain containing protein, and catalase. Subsequent mutant analysis showed that each of these proteins was required for A. baumannii desiccation tolerance. The amino acid sequence of the KGG-domain containing protein predicts that it is an intrinsically disordered protein. Such proteins are critical for desiccation tolerance of the small animals called tardigrades. This protein also has a repeat nucleic acid binding amino acid motif, suggesting that it may protect A. baumannii DNA from desiccation-induced damage.
2022-10-13 | PXD028391 | Pride
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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Project description:A major reservoir for spread of the emerging pathogen Acinetobacter baumannii is hopsital surfaces, where bacteria persist in a desiccated state. To identify gene products influencing desiccation survival, a transposon sequencing (Tn-seq) screen was performed. Using this approach, we identified genes both positively and negatively impacting the desiccation tolerance of A. baumannii.
2022-03-09 | GSE198004 | GEO
Project description:The goal of this Tn-Seq study was to determine important determinants of Acinetobacter baumannii tolerance of sub-MIC concentrations of benzalkonium chloride. This Tn-seq data was then utilized to aide in the determination of the sub-MIC mechanism of action for benzalkonium chloride.
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Project description:Acinetobacter baumannii is an ESKAPE pathogen that rapidly develops resistance to antibiotics and persists for extended periods in the host or on abiotic surfaces. Survival in environmental stress such as phosphate scarcity, represents a clinically significant challenge for nosocomial pathogens. In the face of phosphate starvation, certain bacteria encode adaptive strategies, including the substitution of glycerophospholipids with phosphorus-free lipids. In bacteria, phosphatidylethanolamine, phosphatidylglycerol, and cardiolipin are conserved glycerophospholipids that form lipid bilayers. Here, we demonstrate that in response to phosphate limitation, conserved regulatory mechanisms induce aminolipid production in A. baumannii. Specifically, phosphate limitation induces formation of three lipids, including amine-containing ornithine and lysine aminolipids. We show that phospahte limitation induced transcription of the olsB gene. Mutations that inactivate aminolipid biosynthesis exhibit fitness defects relative to wild type in colistin growth and killing assays.
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Project description:Comparison for gene expression of Acinetobacter baumannii NCCP 16007 by evolved strains
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Project description:Proteomic analysis of Acinetobacter baumannii grown at two different incubation temperatures
2017-10-25 | MSV000081647 | MassIVE
Project description:We performed RNAseq for gene expression analysis for six strains of Acinetobacter Baumannii isolated from blood samples (defined as strains 1, 2, 3, 4 and 6) of patients hospitalized at the University Hospital \\"San Giovanni di Dio e Ruggi d'Aragona\\" (Salerno, Italy)
2023-09-01 | E-MTAB-13274 | biostudies-arrayexpress
Project description:Comparison for gene expression of Acinetobacter baumannii Lab-WT under blue light irradiation
2022-01-31 | GSE195643 | GEO