Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR272374_1.fastq.gz | Fastqsanger.gz | |||
| ERR272374_2.fastq.gz | Fastqsanger.gz |
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Project description:Pseudomonas aeruginosa is an opportunistic pathogen known to cause both acute and chronic infections. P. aeruginosa often encounters hypoxic/anoxic environments within the host, which increases its tolerance to many conventional antibiotics. Towards identifying novel therapeutic treatments, we have been exploring the potential of chlorate, a pro-drug that kills hypoxic/anoxic, antibiotic-tolerant P. aeruginosa populations. Chlorate kills P. aeruginosa when it is enzymatically reduced by hypoxically-induced nitrate reductase, thereby generating the toxic oxidizing agent, chlorite. To better assess its therapeutic potential, we investigated mechanisms of chlorate toxicity and resistance in P. aeruginosa. We combined transposon mutagenesis and high-throughput sequencing to identify genes that alter P. aeruginosa fitness during chlorate treatment. We found that methionine sulfoxide reductase (msr) genes, whose products repair oxidized methionine residues, support survival during chlorate stress. We showed that chlorate treatment leads to proteome-wide methionine oxidation, which is exacerbated in a ∆msrA∆msrB strain. Highly abundant proteins were the likeliest targets of methionine oxidation, including proteins that are abundant under standard conditions (e.g. ribosomes) and proteins that increase in abundance in response to chlorate stress (e.g. protein chaperones). The addition of exogenous methionine partially rescued P. aeruginosa survival during chlorate treatment, suggesting that widespread methionine oxidation contributes to cell death. Finally, we found that decreased nitrate reductase activity is a common mechanism of chlorate resistance. Because nitrate respiration likely sustains P. aeruginosa anaerobic growth and survival within the host, developing chlorate resistance would be expected to hinder pathogen fitness in such environments.
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Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
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Project description:The study investigated the ability of selected (hyper-)thermophilic prokaryotes to grow anaerobically by the reduction of perchlorate and chlorate. Physiological, genomic and proteome analyses suggest that the Crenarchaeon Aeropyrum pernix reduces (per)chlorate with a periplasmic enzyme related to nitrate reductases, while it lacks a functional chlorite-disproportionating enzyme (Cld). A. pernix seems to rely on the chemical reactivity of reduced sulfur compounds with the toxic intermediate chlorite to complete the pathway. The chemical oxidation of thiosulfate (in excessive amounts present in the medium) to sulfate and the concomitant release of chloride anions from the reduction of chlorite are the products of a biotic-abiotic (per)chlorate reduction pathway in A. pernix. The apparent absence of Cld in two other (per)chlorate-reducing microorganisms and their dependence on sulfide for (per)chlorate reduction is consistent with earlier-made observations on (per)chlorate-reducing Archaeoglobus fulgidus. All here discussed microorganisms use strategies for complete (per)chlorate reduction that differ from the physiology of classical (per)chlorate-reducing mesophiles.
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