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Inactivation of farR Causes High Rhodomyrtone Resistance and Increased Pathogenicity in Staphylococcus aureus
Minh-Thu Nguyen1,2, Jongkon Saising1,3, Paula Maria Tribelli1,4
1Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine Tübingen (IMIT), University of Tübingen, Tübingen, Germany.
Frontiers in Microbiology
|June 14, 2019
Summary
A mutation in the Staphylococcus aureus FarR regulator causes resistance to the antibiotic Rhodomyrtone by upregulating the FarE efflux pump. This mutation also increases bacterial virulence, making the bacteria more dangerous.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Rhodomyrtone (Rom) is an acylphloroglucinol antibiotic effective against Gram-positive bacteria.
- Its precise mechanism of action and resistance pathways are not fully understood.
Purpose of the Study:
- To investigate the mechanism of Rhodomyrtone resistance in Staphylococcus aureus.
- To characterize the genetic basis and consequences of Rhodomyrtone resistance.
Main Methods:
- Isolation and characterization of a Rhodomyrtone-resistant mutant (RomR) from Staphylococcus aureus HG001.
- Whole-genome sequencing and comparative transcriptome analysis.
- Gene deletion and complementation experiments.
- Assessment of bacterial virulence in a mouse infection model.
Main Results:
- A single point mutation in the farR gene (Cys116Arg) confers Rhodomyrtone resistance.
- Mutated farR leads to upregulation of its own gene, farE, and global regulators agr and sarA.
- Overexpression of the FarE efflux pump is the primary mechanism of Rhodomyrtone resistance.
- The RomR mutant exhibits increased cytotoxicity and pathogenicity due to agr and sarA upregulation.
Conclusions:
- FarR is a key regulator controlling fatty acid resistance and virulence in Staphylococcus aureus.
- FarE-mediated efflux is crucial for Rhodomyrtone resistance.
- The identified farR mutation results in a hyper-virulent, antibiotic-resistant Staphylococcus aureus strain.
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