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Campylobacter jejuni  is a major food-borne pathogen and a common causative agent of human enterocolitis. Fluoroquinolones are a key class of antibiotics prescribed for clinical treatment of enteric infections including campylobacteriosis, but fluoroquinolone-resistant  Campylobacter  readily emerges under the antibiotic selection pressure. To understand the mechanisms involved in the development of fluoroquinolone-resistant C ampylobacter , we compared the gene expression profiles of  C. jejuni  in the presence and absence of ciprofloxacin using DNA microarray. Our analysis revealed that multiple genes showed significant changes in expression in the presence of a suprainhibitory concentration of ciprofloxacin. Most importantly, ciprofloxacin induced the expression of  mfd , which encodes a transcription-repair coupling factor involved in strand-specific DNA repair. Mutation of the  mfd  gene resulted in an approximately 100-fold reduction in the rate of spontaneous mutation to ciprofloxacin resistance, while overexpression of  mfd  elevated the mutation frequency. In addition, loss of  mfd  in  C. jejuni  significantly reduced the development of fluoroquinolone-resistant  Campylobacter  in culture media or chickens treated with fluoroquinolones. These findings indicate that Mfd is important for the development of fluoroquinolone resistance in  Campylobacter , reveal a previously unrecognized function of Mfd in promoting mutation frequencies, and identify a potential molecular target for reducing the emergence of fluoroquinolone-resistant  Campylobacter .

Key Role of Mfd in the Development of Fluoroquinolone Resistance in Campylobacter jejuni