Bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA325878 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR3743080.fastq.gz | Fastqsanger.gz | |||
| SRR3743081.fastq.gz | Fastqsanger.gz | |||
| SRR3743082_1.fastq.gz | Fastqsanger.gz | |||
| SRR3743082_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 17 |
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Project description:Plasmids are extrachromosomal genetic elements commonly found in bacteria. Plasmids are known to fuel bacterial evolution through horizontal gene transfer (HGT), but recent analyses indicate that they can also promote intragenomic adaptations. However, the role of plasmids as catalysts of bacterial evolution beyond HGT remains poorly explored. In this study, we investigate the impact of a widespread conjugative plasmid, pOXA-48, on the evolution of various multidrug-resistant clinical enterobacteria. Combining experimental and within-patient evolution analyses, we unveil that plasmid pOXA-48 promotes bacterial evolution through the transposition of plasmid-encoded IS1 elements. Specifically, IS1-mediated gene inactivations expedite the adaptation rate of clinical strains in vitro and foster within-patient adaptation in the gut. We decipher the mechanism underlying the plasmid-mediated surge in IS1 transposition, revealing a negative feedback loop regulated by the genomic copy number of IS1. Given the overrepresentation of IS elements in bacterial plasmids, our findings propose that plasmid-mediated IS transposition represents a crucial mechanism for swift bacterial adaptation.
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Project description:Shotgun Proteomic Analysis of ESBL and non ESBL Producing Klebsiella Pneumoniae Clinical Isolates
2021-04-16 | PXD011693 | Pride
Project description:Shotgun Proteomic Analysis of ESBL and non ESBL Producing Klebsiella Pneumoniae Clinical Isolates
2022-02-24 | PXD011558 | Pride
Project description:Unknown are the mechanisms of tolerance and persistence associated to several compounds in A.baumannii clinical isolates. Using transcriptomical and microbiological studies, we found a link between bacterial tolerance mechanisms to clorhexidine as well as the development of persistence in presence of imipenem in an A.baumannii strain belonging to ST-2 clinical clone (carbapenem-resistant with OXA-24 ß-lactamase and AbkAB TA system by plasmid). Interestingly, in A.baumannii ATCC17978 strain (carbapenem-susceptible isolate which carries AbkAB TA system by plasmid) showed persistence in presence of imipenem.
2018-02-09 | GSE110207 | GEO
Project description:Purpose: We investigate the evolutionary footprints of a bacteria-plasmid association consisting of Escherichia coli K-12 MG1655 and plasmid RP4 undergoing a long-term sub-MIC antibiotic stress. Methods: Bacterial mRNA profiles of evolved RP4-carrying strains (E:H:p) and ancestral RP4-carrying strains (A:H:p) were generated by deep sequencing on an Illumina Hiseq platform. The sequence reads that passed quality filters were analyzed by Burrows–Wheeler Aligner (BWA), followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: Using an optimized data analysis workflow, we mapped about 15 million sequence reads of E:H:p and 12 million sequence reads of A:H:p to the E. coli MG1655 genome (GCF_000801205.1) and differential expressed genes were identified with TopHat workflow. RNA-seq data showed that approximately 15% of the transcripts showed differential expression between the E:H:p and A:H:p strains, with a fold change ≥1 and p value <0.005. Altered expression of 26 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Data analysis with bowtie and TopHat workflows provided complementary insights in transcriptome profiling. Conclusions: Our study showed the coevolved bacteria-plasmid pairs has colonization traits superior to the wild-type parent strain. Antibiotic stress was necessary for bacterial evolution and evolved strains mostly employed transcriptional modifications to reduce plasmid-related cost in evolutionary adaptations. Several genes related to chromosome-encoded efflux pumps were transcriptionally upregulated, while most plasmid-harboring genes were downregulated based on RNA gene sequencing. These transcriptional modifications endowed evolved strains with resistant phenotype modifications, including the enhanced bacterial growth and biofilm formation.
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Project description:Background: It remains unclear how high-risk Escherichia coli lineages, like sequence type (ST) 131, initially adapt to carbapenem exposure in its progression to becoming carbapenem resistant. Methods: Carbapenem mutation frequency was measured in multiple subclades of extended-spectrum β-lactamase (ESBL) positive ST131 clinical isolates using a fluctuation assay followed by whole genome sequencing (WGS) characterization. Genomic, transcriptomic, and porin analyses of ST131 C2/H30Rx isolate, MB1860, under prolonged, increasing carbapenem exposure was performed using two distinct experimental evolutionary platforms to measure fast vs. slow adaptation. Results: All thirteen ESBL positive ST131 strains selected from a diverse (n=184) ST131 bacteremia cohort had detectable ertapenem (ETP) mutational frequencies with a statistically positive correlation between initial ESBL gene copy number and mutation frequency (r = 0.87, P<1e-5). WGS analysis of mutants showed initial response to ETP exposure resulted in significant increases in ESBL gene copy numbers or mutations in outer membrane porin (Omp) encoding genes in the absence of ESBL gene amplification with subclade specific adaptations. In both experimental evolutionary platforms, MB1860 responded to initial ETP exposure by increasing blaCTX-M-15 copy numbers via modular, insertion sequence 26 (IS26) mediated pseudocompound transposons (PCTns). Transposase activity driven by PCTn upregulation was a conserved expression signal in both experimental evolutionary platforms. Stable mutations in Omp encoding genes were detected only after prolonged increasing carbapenem exposure consistent with clinical observations. Conclusions: ESBL gene amplification is a conserved response to initial carbapenem exposure, especially within the high-risk ST131 C2 subclade. Targeting such amplification could assist with mitigating carbapenem resistance development.
2024-08-04 | GSE273456 | GEO
Project description:Plasmids are one of the important mobile genetic elements in bacterial evolution. In this study, to evaluate the generality of the impact of plasmid carriage on host cell between different plasmids, we compared the response of Pseudomonas putida KT2440 to harboring three natural plasmids; RP4 (IncP-1, multidrug resistance, 60,099-bp), pCAR1 (IncP-7, carbazole-degradative, 200,231-bp) and NAH7 (IncP-9, naphthalene-degradative, 82,232-bp). We prepared two sets of plasmid-harboring strains from independent conjugation events to elucidate the reproducibility of the impact of the plasmid carriage. As results, the fitness was reduced by the carriage of RP4 and pCAR1 in liquid medium, while it was unaffected or even improved for NAH7-harboring strains. RP4-harboring KT2440 formed smaller colonies than the plasmid-free strain on solid medium (1.6% agar). The host cells were elongated by the carriage of the all plasmids, respectively. Copy number determination by quantitative PCR showed that the amount of each plasmid DNA in the host cell did not differed drastically. Whole genome resequencing showed that 13 SNPs (RP4), 24 SNPs (pCAR1) and 5 SNPs (NAH7) were the total differences between the two substrains for each plasmid-harboring strains. Transcriptome analyses showed that the impact of plasmid carriage was constantly larger in RP4-harboring strain than the other two plasmid-harboring strains. Genes involved in metal acquisition and metabolism were commonly affected by the carriage of the three plasmid. Indeed, plasmid-harboring strains showed greater growth inhibition than plasmid-free strains under iron-limiting condition. This feature could become future target to control plasmid spreading.
2018-02-17 | GSE110733 | GEO
Project description:Many species of pathogenic bacteria harbor critical plasmid-encoded virulence factors, and yet the regulation of plasmid replication is often poorly understood despite playing key role in plasmid-encoded gene expression. Human pathogenic Yersinia, including the plague agent Yersinia. pestis and its close relative Y. pseudotuberculosis, require the type III secretion system (T3SS) virulence factor to subvert host defense mechanisms and colonize host tissues. The Yersinia T3SS is encoded on the IncFII plasmid for Yersinia virulence (pYV). Several layers of gene regulation enables a large increase in expression of Yersinia T3SS genes at mammalian body temperature. Surprisingly, T3SS expression is also controlled at the level of gene dosage. The number of pYV molecules relative to the number of chromosomes per cell, referred to as plasmid copy number, increases with temperature. The ability to increase and maintain elevated pYV plasmid copy number, and therefore T3SS gene dosage, at 37˚C is important for Yersinia virulence. In addition, pYV is highly stable in Yersinia at all temperatures, despite being dispensable for growth outside the host. Yet how Yersinia reinforces elevated plasmid replication and plasmid stability remains unclear. In this study, we show that the chromosomal gene pcnB encoding the polyadenylase PAP I is required for regulation of pYV plasmid copy number (PCN), maintenance of pYV in the bacterial population outside the host, robust T3SS activity, and Yersinia virulence in a mouse infection model. Likewise, pcnB/PAP I is also required for robust expression of the Shigella flexneri virulence plasmid-encoded T3SS that, similar to Yersinia, is encoded on a virulence plasmid whose replication is regulated by sRNA. Furthermore, Yersinia and Shigella pcnB/PAP I is required for maintaining normal PCN of model antimicrobial resistance (AMR) plasmids whose replication is regulated by sRNA, thereby increasing antibiotic resistance by ten-fold. These data suggest that pcnB/PAP I contributes to the spread and stabilization of sRNA-regulated virulence and AMR plasmids in bacterial pathogens, and is essential in maintaining the gene dosage required to mediate plasmid-encoded traits. Importantly pcnB/PAP I has been bioinformatically identified in many species of bacteria despite being studied in only a few species to date. Our work highlights the potential importance of pcnB/PAP I in antibiotic resistance, and shows for the first time that pcnB/PAP I reinforces PCN andpromotes virulence plasmid stability in natural pathogenic hosts with a direct impact on bacterial virulence.
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