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Transcriptomic analysis of acquired resistance to a novel trimethoprim-based photoswitchable antibiotic in Escherichia coli CS1562

ABSTRACT: Transcriptomic analysis of acquired resistance to a novel trimethoprim-based photoswitchable antibiotic in Escherichia coli CS1562

PROVIDER: PRJNA715103 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13987585_1.fastq.gz	Fastqsanger.gz
	SRR13987585_2.fastq.gz	Fastqsanger.gz
	SRR13987586_1.fastq.gz	Fastqsanger.gz
	SRR13987586_2.fastq.gz	Fastqsanger.gz
	SRR13987587_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of acquired resistance to a novel trimethoprim-based photoswitchable antibiotic in Escherichia coli CS1562

Project description:Effect of three different antimicrobial compounds, trimethoprim(TMP), cis-tetra-ortho-chloroazobenzene-trimethoprim (TCATa) and trans-tetra-ortho-chloroazobenzene-trimethoprim (TCATd) , on the resistance development and transcriptome of the E. coli strain CS1562. In addition, acontrol sample was taken along of the propagated parent strain (CS1562) without the addition of any compounds.

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Project description:Fosfomycin is a bactericidal antibiotic, analogous to phosphoenolpyruvate (PEP) that exerts its activity by inhibiting the activity of MurA. This enzyme catalyzes the first step of peptidoglycan biosynthesis, the transfer of enolpyruvate from PEP to uridine- diphosphate-N-acetylglucosamine. Fosfomycin is increasingly used in the last years, mainly for treating infections caused by Gram-negative multidrug resistant bacteria as Stenotrophomonas maltophilia, an opportunistic pathogen characterized by its low susceptibility to antibiotics of common use. The mechanisms of mutational resistance to fosfomycin in Stenotrophomonas maltophilia were studied in the current work. None of the mechanisms so far described for other organisms, which include the production of fosfomycin inactivating enzymes, target modification, induction of alternative peptidoglycan biosynthesis pathway and the impaired entrance of the antibiotic, are involved in the acquisition of such resistance by this bacterial species. Rather the unique cause of resistance in the studied mutants is the mutational inactivation of different enzymes belonging to the Embden-Meyerhof-Parnas central metabolism pathway. The amount of intracellular fosfomycin accumulation did not change in any of these mutants showing that neither the inactivation nor the transport of the antibiotic were involved. Transcriptomic analysis also showed that the mutants did not present changes in the expression level of putative alternative peptidoglycan biosynthesis pathway genes neither any related enzyme. Finally, the mutants did not present an increased PEP concentration that might compete with fosfomycin for its binding to MurA. Based on these results, we describe a completely novel mechanism of antibiotic resistance based on the remodeling of S. maltophilia metabolism.

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