RNA-seq analyzes the effect of purA on transcriptome in Escherichia coli during ciprofloxacin treatment.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1241879 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32857619_1.fastq.gz | Fastqsanger.gz | |||
| SRR32857619_2.fastq.gz | Fastqsanger.gz | |||
| SRR32857620_1.fastq.gz | Fastqsanger.gz | |||
| SRR32857620_2.fastq.gz | Fastqsanger.gz | |||
| SRR32857621_1.fastq.gz | Fastqsanger.gz |
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Project description:PurA encodes an adenylosuccinate synthetase that catalyzes the first step in the de novo synthesis of AMP. A deficiency in purA has been found to confer Escherichia coli tolerance to diverse types of antibiotics. To understand the molecular basis of the increased tolerance, we performed RNA-seq analysis to compare the transcriptional profiles of wild-type and ΔpurA mutant strains before and after ciprofloxacin treatment. The data showed that the purA deficiency suppresses transcript levels from NADH:quinone oxidoreductase genes prior to stress exposure, thereby predisposing E. coli to antibiotic tolerance by reducing respiration. During ciprofloxacin exposure, a purA deficiency suppressed a surge in expression of TCA cycle and ATP synthesis genes and the accumulation of intracellular ATP and ROS, thereby conferring bacterial tolerance to diverse antibiotic stresses.
2025-03-25 | GSE292923 | GEO
Project description:RNA-seq analyzes the effect of ptsI on transcriptome in Escherichia coli during ciprofloxacin treatment.
| PRJNA551458 | ENA
Project description:A deficiency in ptsI, encoding a cytoplasmic protein that serves as the gateway for the phosphoenolpyruvate:sugar phosphotransferase system, was found to confer tolerance to diverse types of disinfectants and antimicrobials. To understand the molecular basis of the increased tolerance, we performed RNA-seq analysis to compare the transcriptional profiles of the wild-type and the ΔptsI mutant strains before and after ciprofloxacin treatment. The data showed that cirpofloxacin treatment drastically increased the exprerssion of genes encoding enzymes in the TCA cycle and that the ptsI mutation suppressed the expression of most TCA genes and all ATP synthase genes, but elevated some of the genes involved in glycolysis and the pentose phosphate pathway (PPP) genes. Such transcriptomic alteration reduced stress-induced surge in respiration and accumutaion of toxic reaactive oxygen species, thereby conferring bacterial tolerance to diverse lethal stressors.
2022-05-20 | GSE133439 | GEO
Project description:Here, we show that PURA predominantly resides in the cytoplasm, where it binds to a large set of transcripts. Many of these transcripts change abundance in response to PURA depletion, in parts reflected in altered protein expression levels. A closer inspection of the regulated proteins indicates a role of PURA in immune responses, mitochondrial function, autophagy and processing (P)-body activity.
2022-12-12 | GSE193900 | GEO
Project description:The protein PURA binds to DNA and RNA and has been suggested to be implicated in different cellular functions. Here, we show that PURA predominantly resides in the cytoplasm, where it binds to a large set of transcripts.
2022-12-12 | GSE193901 | GEO
Project description:Kaiser2014 - Salmonella persistence after ciprofloxacin treatment
The model describes the bacterial tolerance to antibiotics. Using a mouse model for Salmonella diarrhea, the authors have found that bacterial persistence occurs in the presence of the antibiotic ciprofloxacin because Salmonella can exist in two different states. One, the fast-growing population that spreads in the host's tissues and the other, slow-growing "persister" population that hide out inside dendritic cells of the host's immune system and cannot be attacked by the antibiotics. However, this can be killed by adding agents that directly stimulate the host's immune defense.
This model is described in the article:
Cecum lymph node dendritic cells harbor slow-growing bacteria phenotypically tolerant to antibiotic treatment.
Kaiser P, Regoes RR, Dolowschiak T, Wotzka SY, Lengefeld J, Slack E, Grant AJ, Ackermann M, Hardt WD.
PLoS Biol. 2014 Feb 18;12(2):e1001793.
Abstract:
In vivo, antibiotics are often much less efficient than ex vivo and relapses can occur. The reasons for poor in vivo activity are still not completely understood. We have studied the fluoroquinolone antibiotic ciprofloxacin in an animal model for complicated Salmonellosis. High-dose ciprofloxacin treatment efficiently reduced pathogen loads in feces and most organs. However, the cecum draining lymph node (cLN), the gut tissue, and the spleen retained surviving bacteria. In cLN, approximately 10%-20% of the bacteria remained viable. These phenotypically tolerant bacteria lodged mostly within CD103⁺CX₃CR1⁻CD11c⁺ dendritic cells, remained genetically susceptible to ciprofloxacin, were sufficient to reinitiate infection after the end of the therapy, and displayed an extremely slow growth rate, as shown by mathematical analysis of infections with mixed inocula and segregative plasmid experiments. The slow growth was sufficient to explain recalcitrance to antibiotics treatment. Therefore, slow-growing antibiotic-tolerant bacteria lodged within dendritic cells can explain poor in vivo antibiotic activity and relapse. Administration of LPS or CpG, known elicitors of innate immune defense, reduced the loads of tolerant bacteria. Thus, manipulating innate immunity may augment the in vivo activity of antibiotics.
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2024-09-02 | BIOMD0000000527 | BioModels
Project description:The protein PURA binds to DNA and RNA and has been suggested to be implicated in different cellular functions. Here, we show that PURA predominantly resides in the cytoplasm, where it binds to a large set of transcripts.
2022-12-12 | GSE193902 | GEO
Project description:The RNA-binding protein PURA has been implicated in the rare, monogenetic, neurodevelopmental disorder PURA Syndrome. PURA binds both DNA and RNA and has been associated with various cellular functions. Only little is known about its main cellular functions and the molecular pathways affected upon PURA depletion. Here, we show that PURA is predominantly located in the cytoplasm, where it binds to thousands of mRNAs. Many of these transcripts change abundance in response to PURA depletion. The encoded proteins suggest a role for PURA in immune responses, mitochondrial function, autophagy and processing (P)-body activity. Intriguingly, reduced PURA levels decrease the expression of the integral P-body components LSM14A and DDX6, and strongly affect P-body formation in human cells. Furthermore, PURA knockdown results in stabilization of P-body-enriched transcripts, whereas other mRNAs decrease. Hence, reduced PURA levels, as reported in patients with PURA Syndrome, influence the formation and composition of this phase-separated RNA processing machinery. Our study on PURA provides a blueprint for the comprehensive understanding of the tight connection between P-body-associated RNA regulation and neurodevelopmental disorders.
2022-12-19 | PXD030266 | Pride