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Mechanistic Divergence Between SOS Response Activation and Antibiotic-Induced Plasmid Conjugation in E. coli

ABSTRACT: Project description: Plasmids, frequently carried by environmental and pathogenic bacteria, play a critical role in rapid dissemination of antibiotic resistance through conjugation. The use of antibiot-ics further induces this conjugative transmission between bacteria and thereby plays a role in the rise of antibiotic resistance. This highlights the need for a fundamental understanding of the regu-lation of transmission, to limit the problem. In addition, antibiotics induce the bacterial SOS re-sponse, however, whether using SOS as target can reduce conjugation, has been unclear. In this research, we used SOS-inducing compounds, SOS-mutants, conjugation and proteomics, and showed that antibiotic induced conjugation and induction of the SOS response happens through different mechanisms. This provides a new insight, which affects future strategies to control the spread of antibiotics.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Escherichia Coli

SUBMITTER: Arkadiusz Nawrocki

LAB HEAD: Line Elnif Thomsen, Associate professor M.Sc. PhD

PROVIDER: PXD063721 | Pride | 2025-05-08

REPOSITORIES: Pride

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	MRL_AN_E3_20230224_Ruoxuan-JMJ_HpH-01.raw	Raw
	MRL_AN_E3_20230224_Ruoxuan-JMJ_HpH-02.raw	Raw
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	MRL_AN_E3_20230224_Ruoxuan-JMJ_HpH-05.raw	Raw

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Treatment with Cefotaxime Affects Expression of Conjugation Associated Proteins and Conjugation Transfer Frequency of an IncI1 Plasmid in Escherichia coli

Project description:Horizontal gene transfer (HGT) is the major mechanism responsible for spread of antibiotic resistance. Antibiotic treatment has been suggested to promote HGT, either by directly affecting the conjugation process itself or by selecting for conjugations subsequent to DNA transfer. However, recent research suggests that the effect of antibiotic treatment on plasmid conjugation frequencies, and hence the spread of resistance plasmids, may have been overestimated. We addressed the question by quantifying transfer proteins and conjugation frequencies of a blaCTX-M-1 encoding IncI1 resistance plasmid in Escherichia coli MG1655 in the presence and absence of therapeutically relevant concentrations of cefotaxime (CTX). Analysis of the proteome by iTRAQ labeling and liquid chromatography tandem mass spectrometry revealed that Tra proteins were significantly up regulated in the presence of CTX. The up-regulation of the transfer machinery was confirmed at the transcriptional level for five selected genes. The CTX treatment did not cause induction of the SOS39 response as revealed by absence of significantly regulated SOS associated proteins in the proteome and no significant up-regulation of recA and sfiA genes. The frequency of plasmid conjugation, measured in an antibiotic free environment, increased significantly when the donor was pre-grown in broth containing CTX compared to growth without this drug, regardless of whether blaCTX-M-1 was located on the plasmid or in trans on the chromosome. The results shows that antibiotic treatment can affect expression of a plasmid conjugation machinery and subsequent DNA transfer.

2017-11-21 | PXD006679 | Pride

RNA polymerase stalling-derived genome instability underlies ribosomal antibiotic efficacy and resistance evolution

Project description:Bacteria often evolve antibiotic resistance through mutagenesis. However, the processes causing the mutagenesis have not been fully resolved. Here we found that a broad range of ribosome-targeting antibiotics caused mutations through an underexplored pathway. Focusing on the clinically important aminoglycoside gentamicin, we found that the translation inhibitor caused genome-wide premature stalling of RNA polymerase (RNAP) in a loci-dependent manner. Further analysis showed that the stalling was caused by disruption of transcription-translation coupling. Anti-intuitively, the stalled RNAPs subsequently induced lesions to the DNA via transcription-coupled repair. While most of the bacteria were killed by genotoxicity, a small subpopulation acquired mutations via SOS-induced mutagenesis. Given that these processes were triggered shortly after antibiotic addition, resistance rapidly emerged in the population. Our work revealed a new mechanism of action of ribosomal antibiotics, illustrates the importance of dissecting the complex interplay between multiple molecular processes in understanding antibiotic efficacy, and suggests new strategies for countering the development of resistance.

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2015-01-26 | E-GEOD-60568 | biostudies-arrayexpress

Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut (LMD)

Project description:We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria. This series includes gene expression of the laser microdissected compartments of the ileum such as villous epithelium, lamina propria and crypts from specific pathogen free mice common reference design with a pool of small intestine RNA labeled with Cy3

2015-01-26 | E-GEOD-60567 | biostudies-arrayexpress

High-throughput identification of the impact of ΔrecA mutation on sensitivities to various chemical compounds in Escherichia coli

Project description:Antibiotic resistance is currently considered as a global threat to public health. It was shown that adaptive resistance mutation and acquisition of resistance genes by horizontal gene transfer are facilitated by RecA-dependent SOS response during antibiotic treatment. In this study, we performed high-throughput determination of minimal inhibitory concentrations (MICs) of 214 chemicals including not only various kinds of antibiotics but also toxic chemicals of unknown drug action in Escherichia coli wild-type MDS42 strain and the ΔrecA mutant strain. The ΔrecA mutant showed increased sensitivity to DNA-damaging agents, DNA replication inhibitors, and chromate stress. The ΔrecA mutant also showed increased sensitivity to chemicals other than DNA-damaging agents such as S-(2-aminoethyl)- l-cysteine, l-histidine, ruthenium red, D-penicillamine, carbonyl cyanide 3-chlorophenylhydrazone (CCCP), cerulenin, and l-cysteine. Microarray analysis showed that expressions of glnK, nac, and glnLG encoding nitrogen assimilation regulators together with amtB encoding ammonium transporter decreased in the ΔrecA mutant strain. These results suggest that ΔrecA mutation affect not only SOS response but also nitrogen assimilation.

2019-02-24 | GSE121218 | GEO

RNA-seq analysis of the transfer of R388 plasmid with or without ardC, from E. coli to P. putida

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Molecular Responses During Bacterial Filamentation Induced by Antibiotics

Project description:Bacterial filamentation is one of the most important bacterial SOS responses to antibiotic drugs and contributes to the development of antimicrobial resistance. Understanding the mechanism of the bacterial SOS response is crucial to control the development of antibiotic-resistant bacteria. We uncover the molecular changes of SOS-associated bacterial filamentation. Bacterial proteins that correlate with bacterial SOS responses and facilitate to bacterial antimicrobial resistance are studied.

2023-01-04 | PXD039235 |

Sublethal concentrations of antibiotics cause shift to anaerobic metabolism in Listeria monocytogenes and induce phenotypes linked to antibiotic tolerance

Project description:The human pathogenic bacterium Listeria monocytogenes was exposed to antibiotics both during clinical treatment and as a saprophyte. As one of the keys to successful treatment is continued antibiotic sensitivity, the purpose of this study was to determine if exposure to sublethal antibiotic concentrations would affect the bacterial physiology and potentially induce tolerance to antibiotics. Transcriptomic analyses demonstrated that each of four antibiotics caused a compound-specific gene expression pattern related to (the) mode-of-action of the particular antibiotic. All four antibiotics caused the same changes in expression of several metabolic genes indicating a shift from aerobic to anaerobic metabolism driven by the induction of lmo1634 and the repression of alsA and lmo1992. This shift in metabolism could be a survival strategy in response to antibiotics and is further supported by the observation that a Δlmo1634 mutant was more sensitive to bactericidal antibiotics. The monocin locus encoding a cryptic prophage was induced by co-trimoxazole and repressed by ampicillin and gentamicin. This expression pattern correlated with the observed antibiotic-dependent biofilm formation, indicating a role of monocin in antibiotic-induced biofilm formation and a ΔlmaDCBA mutant confirmed this correlation. Thus, sublethal concentrations of antibiotics caused metabolic and physiological changes indicating that the organism is preparing to withstand lethal concentrations of antibiotics.

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Sublethal concentrations of antibiotics cause shift to anaerobic metabolism in Listeria monocytogenes and induce phenotypes linked to antibiotic tolerance

Project description:The human pathogenic bacterium Listeria monocytogenes was exposed to antibiotics both during clinical treatment and as a saprophyte. As one of the keys to successful treatment is continued antibiotic sensitivity, the purpose of this study was to determine if exposure to sublethal antibiotic concentrations would affect the bacterial physiology and potentially induce tolerance to antibiotics. Transcriptomic analyses demonstrated that each of four antibiotics caused a compound-specific gene expression pattern related to (the) mode-of-action of the particular antibiotic. All four antibiotics caused the same changes in expression of several metabolic genes indicating a shift from aerobic to anaerobic metabolism driven by the induction of lmo1634 and the repression of alsA and lmo1992. This shift in metabolism could be a survival strategy in response to antibiotics and is further supported by the observation that a Îlmo1634 mutant was more sensitive to bactericidal antibiotics. The monocin locus encoding a cryptic prophage was induced by co-trimoxazole and repressed by ampicillin and gentamicin. This expression pattern correlated with the observed antibiotic-dependent biofilm formation, indicating a role of monocin in antibiotic-induced biofilm formation and a ÎlmaDCBA mutant confirmed this correlation. Thus, sublethal concentrations of antibiotics caused metabolic and physiological changes indicating that the organism is preparing to withstand lethal concentrations of antibiotics. Investigation of mRNA and sRNA expression profiles of L. monocytogenes EGD cells exposed to sublethal concentrations of four different antibiotics i.e. ampicillin, tetracycline, gentamicin and co-trimoxazole for 3h.

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