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Whole Genome Sequencing Demonstrates Fidaxomicin is Superior to Vancomycin for Prevention of Clostridium difficile Relapse and Reinfection

ABSTRACT: Whole Genome Sequencing Demonstrates Fidaxomicin is Superior to Vancomycin for Prevention of Clostridium difficile Relapse and Reinfection

PROVIDER: PRJEB4638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR347956_1.fastq.gz	Fastqsanger.gz
	ERR347956_2.fastq.gz	Fastqsanger.gz
	ERR347957_1.fastq.gz	Fastqsanger.gz
	ERR347957_2.fastq.gz	Fastqsanger.gz
	ERR347958_1.fastq.gz	Fastqsanger.gz

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Whole-genome sequencing demonstrates that fidaxomicin is superior to vancomycin for preventing reinfection and relapse of infection with Clostridium difficile.

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Project description:Vancomycin tolerance in multidrug resistance Staphylococcus aureus is correlated with dysregulation of small RNAs although their contribution to antibiotic tolerance in poorly understood. RNA-RNA interactome profiling techniques are expanding our understanding of sRNA-mRNA interactions in bacteria; however, determining the function of these interactions for hundreds of sRNA-mRNA pairs is a major challenge. At steady-state, protein and mRNA abundances are often highly correlated and lower than expected protein abundance may indicate translational repression of an mRNA. We used label-free quantitative proteomics to examine changes in protein expression in vancomycin tolerant S. aureus strain in response to vancomycin treatment. We correlated the protein levels with gene transcript abundance and ribosome occupancy to identify sRNA-mRNA interactions that regulate mRNA translation. We used the machine learning technique self-organising maps (SOMS) to cluster genes with similar transcription and translation patterns and identified a cluster of mRNAs that appeared to be post-transcriptionally repressed. By integrating our clustering analysis with the sRNA-mRNA interactome data generated in vancomycin tolerant S. aureus by RNase III-CLASH, we identified a cluster of sRNAs that may be mediating translational repression. We have confirmed sRNA-dependant post-transcriptional repression of several mRNAs in this cluster. Two of these interactions are mediated by RsaOI, a sRNA that is highly upregulated by vancomycin, and these targets include HPr and the cell-wall autolysin Atl, with only Atl downregulated at the protein level upon vancomycin treatment. These findings suggest RsaOI coordinates carbon metabolism and cell wall turnover during vancomycin treatment

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