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Although cobalt (Co) is indispensable for life, it is toxic to cells when accumulated in excess. The DmeRF system is a well-characterized metal-response system that contributes to Co and nickel resistance in certain bacterial species. The <i>Vibrio parahaemolyticus</i> RIMD 2210633 genome also harbors a <i>dmeRF</i> operon that encodes a multiple antibiotic resistance regulator family transcriptional regulator and a cation diffusion facilitator family protein. Quantitative real-time PCR, growth curves analysis, inductively coupled plasma-mass spectrometry, β-galactosidase activity assays, electrophoretic mobility shift assays, and a mouse infection experiment were performed to characterize the function of the DmeRF system in <i>V. parahaemolyticus</i>. Zinc, copper, and Co significantly increase <i>dmeF</i> expression, with Co inducing the greatest increase. DmeF promotes <i>V. parahaemolyticus</i> growth under high-Co conditions. Additionally, increased accumulation of cellular Co in the Δ<i>dmeF</i> mutant indicates that DmeF is potentially involved in Co efflux. Moreover, DmeR represses the <i>dmeRF</i> operon by binding directly to its promoter in the absence of Co. Finally, the DmeRF system was not required for <i>V. parahaemolyticus</i> virulence in mice. Collectively, our data indicate that the DmeRF system is involved in maintaining Co homeostasis in <i>V. parahaemolyticus</i> and DmeR functioning as a repressor of the operon.