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Genome-wide mapping of fluoroquinolone-induced gyrase cleavage sites displays drug specific effects that correlate with bacterial persistence

ABSTRACT: Genome-wide mapping of fluoroquinolone-induced gyrase cleavage sites displays drug specific effects that correlate with bacterial persistence

PROVIDER: PRJNA851453 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19889800_1.fastq.gz	Fastqsanger.gz
	SRR19889800_2.fastq.gz	Fastqsanger.gz
	SRR19889801_1.fastq.gz	Fastqsanger.gz
	SRR19889801_2.fastq.gz	Fastqsanger.gz
	SRR19889802_1.fastq.gz	Fastqsanger.gz

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Genome-wide mapping of fluoroquinolone-induced gyrase cleavage sites displays drug specific effects that correlate with bacterial persistence

Project description:Persisters are rare phenotypic variants that can survive bactericidal doses of antibiotics and resume growth after the conclusion of treatment. They are suspected to be culprits of recurrent infections, and are distinct from resistant mutants because they are genetically identical to bacteria that die from treatment. Persisters to fluoroquinolones (FQs) experience DNA damage from treatment in stationary-phase culture, which suggests that FQs can corrupt their primary target, DNA gyrase, even in these super-tolerant cells. Since DNA damage from FQs originates from its stabilization of DNA gyrase in complexes with cleaved DNA, we hypothesized that the characteristics of FQ-stabilized DNA gyrase cleavage sites (GCS), such as the abundance, and/or location, might be influential to persistence. To test this hypothesis, we measured genome-wide distributions of GCS after treatment with a panel of FQs.We found drug-specific effects on the location and abundances of GCSs and discovered a negative correlation between the number of GCSs and FQ persister levels. Further, additional experiments and analyses suggested that persister levels are not governed by cleavage to a single specific site, but rather survival is a more complex function with respect to GCSs. Together, these findings demonstrate that there are drug specific differences in GCSs that correlate with persister levels, and suggest that the ability of an FQ to stabilize DNA-gyrase complexes at more sites will improve its bactericidal ability.

2022-12-05 | GSE206608 | GEO

Fluoroquinolone-induced gyrase cleavage sites

Project description:Fluoroquinolone-induced gyrase cleavage sites

| PRJNA851452 | ENA

Genome-wide mapping of fluoroquinolone-stabilized DNA gyrase cleavage sites displays drug specific effects that correlate with bacterial persistence.

Project description:Bacterial persisters are rare phenotypic variants that are suspected to be culprits of recurrent infections. Fluoroquinolones (FQs) are a class of antibiotics that facilitate bacterial killing by stabilizing bacterial type II topoisomerases when they are in a complex with cleaved DNA. In Escherichia coli, DNA gyrase is the primary FQ target, and previous work has demonstrated that persisters are not spared from FQ-induced DNA damage. Since DNA gyrase cleavage sites (GCSs) largely govern the sites of DNA damage from FQ treatment, we hypothesized that GCS characteristics (e.g. number, strength, location) may influence persistence. To test this hypothesis, we measured genome-wide GCS distributions after treatment with a panel of FQs in stationary-phase cultures. We found drug-specific effects on the GCS distribution and discovered a strong negative correlation between the genomic cleavage strength and FQ persister levels. Further experiments and analyses suggested that persistence was unlikely to be governed by cleavage to individual sites, but rather survival was a function of the genomic GCS distribution. Together, these findings demonstrate FQ-specific differences in GCS distribution that correlate with persister levels and suggest that FQs that better stabilize DNA gyrase in cleaved complexes with DNA will lead to lower levels of persistence.

| S-EPMC9943676 | biostudies-literature

Effect of fluoroquinolone-induced gyrase cleavage sites on gene expression during drug treatment period and recovery period on E. coli

2022-12-05 | GSE206609 | GEO

Fluoroquinolone-induced gyrase cleavage sites

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-05 | GSE206610 | GEO

Effect of fluoroquinolone-induced gyrase cleavage sites on gene expression during drug treatment period and recovery period on E. coli

Project description:Effect of fluoroquinolone-induced gyrase cleavage sites on gene expression during drug treatment period and recovery period on E. coli

| PRJNA851455 | ENA

Targeting bacterial gyrase with cystobactamid, fluoroquinolone and aminocoumarin antibiotics induces distinct molecular signatures in Pseudomonas aeruginosa

Project description:The design of novel antibiotics that break antimicrobial resistance relies on a profound understanding of their mechanism of action. While it has been shown that the cellular effects of antibiotics cluster according to their molecular targets, we investigated whether compounds binding to different sites of the same target can be differentiated by their transcriptome or metabolome signatures. The effects of three fluoroquinolones, two aminocoumarins and two cystobactamids, all inhibiting bacterial gyrase, on Pseudomonas aeruginosa at sub-inhibitory concentrations were captured by RNA sequencing.

2021-05-03 | GSE166602 | GEO

Targeting bacterial gyrase with cystobactamid, fluoroquinolone and aminocoumarin antibiotics induces distinct molecular signatures in Pseudomonas aeruginosa

Project description:Targeting bacterial gyrase with cystobactamid, fluoroquinolone and aminocoumarin antibiotics induces distinct molecular signatures in Pseudomonas aeruginosa

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Transcriptional consequences of DNA gyrase inhibition

Project description:DNA gyrase is an essential enzyme whose activity is required for DNA replication and chromosome maintenance. Inhibition of gyrase results in multiple physiological effects including changes in DNA superhelicity, replication arrest and DNA damage. Using genetic, genomic, statistical and biochemical techniques, we have untangled the contribution of individual effects, assessed their relative significance and concluded that: i) DNA replication is required for the formation of spatial transcriptional domains; ii) transcriptional response to gyrase inhibition is coordinated between at least two modules involved in DNA maintenance, relaxation and damage response; iii) genes whose transcriptional response to gyrase inhibition does not depend on the activity of topoisomerase I can be classified on the basis of the GC excess in their upstream and coding sequences into, respectively, activated and repressed by gyrase inhibition; iv) relaxation by topoisomerase I dominates the transcriptional response upon gyrase inhibition, followed by the effects of replication and RecA. Keywords: time course

2006-03-10 | GSE4408 | GEO

Gyrase binding in wild type and gyrA D82G mutant

Project description:Raw data for spatial pattern analysis of gyrase binding in E. coli MG1655 wild type and gyrA D82G mutant (ChIP-chip data) Keywords: other

2004-09-09 | GSE1735 | GEO

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