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Mutations upstream of fabI in triclosan resistant Staphylococcus aureus strains are associated with elevated fabI gene expression

Overview of attention for article published in BMC Genomics, April 2015
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Title
Mutations upstream of fabI in triclosan resistant Staphylococcus aureus strains are associated with elevated fabI gene expression
Published in
BMC Genomics, April 2015
DOI 10.1186/s12864-015-1544-y
Pubmed ID
Authors

Denis Grandgirard, Leonardo Furi, Maria Laura Ciusa, Lucilla Baldassarri, Daniel R Knight, Ian Morrissey, Carlo R Largiadèr, Stephen L Leib, Marco R Oggioni

Abstract

The enoyl-acyl carrier protein (ACP) reductase enzyme (FabI) is the target for a series of antimicrobial agents including novel compounds in clinical trial and the biocide triclosan. Mutations in fabI and heterodiploidy for fabI have been shown to confer resistance in S. aureus strains in a previous study. Here we further determined the fabI upstream sequence of a selection of these strains and the gene expression levels in strains with promoter region mutations. Mutations in the fabI promoter were found in 18% of triclosan resistant clinical isolates, regardless the previously identified molecular mechanism conferring resistance. Although not significant, a higher rate of promoter mutations were found in strains without previously described mechanisms of resistance. Some of the mutations identified in the clinical isolates were also detected in a series of laboratory mutants. Microarray analysis of selected laboratory mutants with fabI promoter region mutations, grown in the absence of triclosan, revealed increased fabI expression in three out of four tested strains. In two of these strains, only few genes other than fabI were upregulated. Consistently with these data, whole genome sequencing of in vitro selected mutants identified only few mutations except the upstream and coding regions of fabI, with the promoter mutation as the most probable cause of fabI overexpression. Importantly the gene expression profiling of clinical isolates containing similar mutations in the fabI promoter also showed, when compared to unrelated non-mutated isolates, a significant up-regulation of fabI. In conclusion, we have demonstrated the presence of C34T, T109G, and A101C mutations in the fabI promoter region of strains with fabI up-regulation, both in clinical isolates and/or laboratory mutants. These data provide further observations linking mutations upstream fabI with up-regulated expression of the fabI gene.

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Mendeley readers

The data shown below were compiled from readership statistics for 57 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
France 1 2%
Switzerland 1 2%
Unknown 55 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 15 26%
Researcher 12 21%
Student > Master 10 18%
Student > Bachelor 7 12%
Student > Doctoral Student 2 4%
Other 5 9%
Unknown 6 11%
Readers by discipline Count As %
Agricultural and Biological Sciences 19 33%
Biochemistry, Genetics and Molecular Biology 12 21%
Medicine and Dentistry 5 9%
Neuroscience 2 4%
Environmental Science 2 4%
Other 9 16%
Unknown 8 14%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 28 January 2016.
All research outputs
#7,173,129
of 8,295,152 outputs
Outputs from BMC Genomics
#5,179
of 5,858 outputs
Outputs of similar age
#280,386
of 334,360 outputs
Outputs of similar age from BMC Genomics
#263
of 287 outputs
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