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Characterisation of the secondary effects of sub-inhibitory concentrations of 1-(1-naphthylmethyl)-piperazine (NMP) in Klebsiella pneumoniae

ABSTRACT: Characterisation of the secondary effects of sub-inhibitory concentrations of 1-(1-naphthylmethyl)-piperazine (NMP) in Klebsiella pneumoniae

PROVIDER: PRJNA505847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8202310.fastq.gz	Fastqsanger.gz
	SRR8202311.fastq.gz	Fastqsanger.gz
	SRR8202312.fastq.gz	Fastqsanger.gz
	SRR8202313.fastq.gz	Fastqsanger.gz
	SRR8202314.fastq.gz	Fastqsanger.gz

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Characterisation of the secondary effects of sub-inhibitory concentrations of 1-(1-naphthylmethyl)-piperazine (NMP) in Klebsiella pneumoniae

Project description:Efflux of antimicrobial compounds from bacterial cells is one of the important mechanisms responsible for multi-drug resistance (MDR). Inhibiting the activity of efflux pumps using chemosensitizers like 1-(1-naphthylmethyl)-piperazine (NMP) is currently considered as a promising strategy to overcome MDR. However, additional effects of NMP other than inhibition are rarely if ever considered. Here, using phenotypic, phenotypic microarray and transcriptomic assays we show that NMP plays a role in membrane destabilization in MDR Klebsiella pneumoniae MGH 78578 strain. The observation of membrane destabilization was supported by RNA-seq data which showed that many up-regulated genes were either directly involved in responses to envelope stress or bacterial repair systems which are essential to maintain viability in an environment containing NMP. Membrane destabilization happens as early as 15 minutes post-NMP treatment. We postulate that the early membrane disruption leads to destabilization of inner membrane potential, impairing ATP production and consequently resulting in efflux pump inhibition.

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Project description:To see the effect of sub-inhibitory concentrations of tobramycin on Pseudomonas aeruginosa grown under aerobic conditions. RNA was isolated form 4 biological repeats of P.aeruginosa grown to mid-log in cationic adjusted mueller hinton broth and 4 biological repeats of P.aeruginosa with the addition of 0.25ug/ml tobramycin in cationic adjusted mueller hinton broth. null

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Genome location dictates the transcriptional response to sub-inhibitory concentrations of PolC-inhibitors in Clostridium difficile

Project description:Genome location dictates the transcriptional response to sub-inhibitory concentrations of PolC-inhibitors in Clostridium difficile

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Genome location dictates the transcriptional response to sub-inhibitory concentrations of PolC-inhibitors in Clostridium difficile

Project description:Clostridium difficile is a potentially lethal gut pathogen that causes nosocomial and community acquired infections. Limited treatment options and reports of reduced susceptibility to current treatment emphasize the necessity for novel antimicrobials. The DNA-polymerase of gram-positive organisms is an attractive target for the development of antimicrobials. ACX362E (N2-(3,4-Dichlorobenzyl)-7-(2-[1-morpholinyl]ethyl)guanine; MorE-DCBG) is a DNA polymerase inhibitor in pre-clinical development as a novel therapeutic against C. difficile infection. This synthetic purine shows preferential activity against C. difficile Pol IIIC over those of other organisms in vitro and is effective in an animal model of C. difficile infection. In this study we have determined its efficacy against a large collection of clinical isolates. At concentrations below the minimal inhibitory concentration, the presumed slowing (or stalling) of replication forks due to ACX362E leads to a growth defect. We have determined the transcriptional response of C. difficile to replication inhibition and observed an overrepresentation of up-regulated genes near the origin of replication in the presence of PolC-inhibitors, but not when cells were subjected to sub-inhibitory concentrations of other antibiotics. This phenomenon can be explained by a gene dosage shift, as we observed a concomitant increase in the ratio between origin-proximal versus terminus-proximal gene copy number upon exposure to PolC-inhibitors. Moreover, we show that certain genes differentially regulated under PolC-inhibition are controlled by the origin-proximal general stress response regulator sigma factor B. Together, these data suggest that genome location both directly and indirectly determines the transcriptional response to replication inhibition in C. difficile

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The mechanism of tigecycline resistance in Acinetobacter baumannii under sub-minimal inhibitory concentration tigecycline

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