Ontology highlight
ABSTRACT:
PROVIDER: PRJNA377846 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MWVR01.dat.gz | Other | |||
| MWVR01.fasta.gz | Fasta.gz | |||
| MWVR01.master.dat | Other | |||
| MWVS01.dat.gz | Other | |||
| MWVS01.fasta.gz | Fasta.gz |
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Project description:Using Nanopore sequencing, our study has revealed a close correlation between genomic methylation levels and antibiotic resistance rates in Acinetobacter Baumannii. Specifically, the combined genome-wide DNA methylome and transcriptome analysis revealed the first epigenetic-based antibiotic-resistance mechanism in A. baumannii. Our findings suggest that the precise location of methylation sites along the chromosome could provide new diagnostic markers and drug targets to improve the management of multidrug-resistant A. baumannii infections.
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Project description:Ni Contaminated soil antibiotic resistance genes study
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Project description:Antibiotic treatment typically eliminates a significant portion of a bacterial population, leaving behind a smaller subset of tolerant cells that can survive the treatment. These tolerant cells hinder the effectiveness of the antibiotic, potentially leading to the development of antibiotic resistance within the population. Antibiotic tolerance differs from resistance: tolerant cells are unable to grow or reproduce in the presence of the antibiotic, but they can proliferate once the antibiotic is removed. However, in cases of resistance, the antibiotic loses its efficacy entirely, posing a significant threat to public health. Our study challenges the long-held consensus that persisters are completely dormant and are of one single population. Our results clearly show that persisters are not as dormant as once thought, and multiple populations of persisters form during lethal antibiotic treatment despite the cells being genetically identical. We compared the transcriptome profiles at different time points to investigate the dynamic changes and/or existence of multiple persister subpopulations in response to lethal antibiotic ampicillin (Amp) and ciprofloxacin (Cip) treatment in E. coli.
2024-06-21 | GSE256167 | GEO
Project description:We used a DNA microarray chip covering 369 resistance types to investigate the relation of antibiotic resistance gene diversity with humans’ age. Metagenomic DNA from fecal samples of 123 healthy volunteers of four different age groups, i.e. pre-school Children (CH), School Children (SC), High School Students (HSS) and Adults (AD) were used for hybridization. The results showed that 80 different gene types were recovered from the 123 individuals gut microbiota, among which 25 were present in CH, 37 in SC, 58 in HSS and 72 in AD. Further analysis indicated that antibiotic resistance genes in groups of CH, SC and AD can be independently clustered, and those ones in group HSS are more divergent. The detailed analysis of antibiotic resistance genes in human gut is further described in the paper DNA microarray analysis reveals the antibiotic resistance gene diversity in human gut microbiota is age-related submitted to Sentific Reports
2014-01-16 | GSE54070 | GEO
Project description:With the global increase in the use of carbapenems, several gram-negative bacteria have acquired carbapenem resistance, thereby limiting treatment options. Klebsiella pneumoniae is one of such notorious pathogen that is being widely studied to find novel resistance mechanisms and drug targets. These antibiotic-resistant clinical isolates generally harbor many genetic alterations, and identification of causal mutations will provide insights into the molecular mechanisms of antibiotic resistance. We propose a method to prioritize mutated genes responsible for antibiotic resistance, in which mutated genes that also show significant expression changes among their functionally coupled genes become more likely candidates. For network-based analyses, we developed a genome-scale co-functional network of K. pneumoniae genes, KlebNet (www.inetbio.org/klebnet). Using KlebNet, we could reconstruct functional modules for antibiotic-resistance, and virulence, and retrieved functional association between them. With complementation assays with top candidate genes, we could validate a gene for negative regulation of meropenem resistance and four genes for positive regulation of virulence in Galleria mellonella larvae. Therefore, our study demonstrated the feasibility of network-based identification of genes required for antimicrobial resistance and virulence of human pathogenic bacteria with genomic and transcriptomic profiles from antibiotic-resistant clinical isolates.
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Project description:In a given bacterial population, antibiotic treatment kills a large portion of the population, while a small, tolerant subpopulation survives. Tolerant cells disrupt the efficacy of antibiotic treatment and increase the likelihood that a population gains antibiotic resistance. Antibiotic tolerance is different from resistance because tolerant cells cannot grow and replicate in the presence of the antibiotic, but when the antibiotic is removed, they begin to propagate. When a population becomes resistant, the antibiotic becomes ineffective, which is a major health concern. Since antibiotic tolerance often leads to antibiotic resistance, we have taken a systems biology approach to examine how regulatory networks respond to antibiotic stress so that cells can survive and recover after antibiotic treatment. We have compared gene expression with and without ampicillin in E. coli.
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Project description:Understanding constraints which shape antibiotic resistance is key for predicting and controlling drug resistance. Here, we performed high-throughput laboratory evolution of Actinobacillus pleuropneumoniae and its ciprofloxacin resistance-inducing derivatives.This study aims to explore the mechanism of acquired ciprofloxacin resistance in Actinobacillus pleuropneumoniae.
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Project description:Cationic antimicrobial peptides (CAPs) are promising novel alternatives to conventional antibacterial agents, but the overlap in resistance mechanisms between small-molecule antibiotics and CAPs is unknown. Does evolution of antibiotic resistance decrease (cross-resistance) or increase (collateral sensitivity) susceptibility to CAPs? We systematically addressed this issue by studying the susceptibilities of a comprehensive set of antibiotic resistant Escherichia coli strains towards 24 antimicrobial peptides. Strikingly, antibiotic resistant bacteria frequently showed collateral sensitivity to CAPs, while cross-resistance was relatively rare. We identified clinically relevant multidrug resistance mutations that simultaneously elevate susceptibility to certain CAPs. Transcriptome and chemogenomic analysis revealed that such mutations frequently alter the lipopolysaccharide composition of the outer cell membrane and thereby increase the killing efficiency of membrane-interacting antimicrobial peptides. Furthermore, we identified CAP-antibiotic combinations that rescue the activity of existing antibiotics and slow down the evolution of resistance to antibiotics. Our work provides a proof of principle for the development of peptide based antibiotic adjuvants that enhance antibiotic action and block evolution of resistance.
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Project description:This study reports on the co-administration of a zinc ionophore (PBT-2) and ampicillin to break antibiotic resistance of Streptococcus pneumoniae in a murine pneumonia model. The molecular mechanism for this heightened antimicrobial activity was identified through transcriptomic and metabolomic analyses of a wild type strain and a zinc efflux mutant to identify cellular targets of zinc intoxication. This revealed that zinc intoxication induces numerous cellular disruptions, which when combined with frontline antibiotics, can break antibiotic resistance and potentially preclude further resistance from emerging.
2022-02-01 | GSE159901 | GEO