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Background  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.    Results  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 .    Conclusions  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.    Electronic supplementary material  The online version of this article (doi:10.1186/s12864-015-1544-y) contains supplementary material, which is available to authorized users.

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