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ABSTRACTMetals are nutrients essential for almost all lifeforms. Bacteria have evolved several mechanisms to overcome the metal restrictions imposed by the host. Vibrio parahaemolyticuscauses severe threats to public health and significant economic losses in shrimp aquaculture. Herein, we report that ZrgA contributes to zinc acquisition in this pathogen. The operon VP_RS01455to VP_RS01475of V. parahaemolyticusencodes the putative Zn transporter ZrgABCDE, whose homologs are widely distributed in Vibrionaceae. RNA sequencing analysis revealed that V. parahaemolyticusmodulates the transcriptome in response to Zn limitation. Genes in the Zinc uptake regulator (Zur) regulon are upregulated during Zn limitation, including three genes annotated to encode Zn-binding proteins. Significant upregulation of these three genes during Zn limitation was also confirmed by quantitative real-time PCR (qRT-PCR) analysis. However, only the mutants containing a VP_RS01470(zrgA) deletion exhibited impaired growth under Zn-deficient conditions, indicating that VP_RS01470plays the predominant role in V. parahaemolyticusZn acquisition. The VP_RS01470deletion mutant displayed a false appearance of decreased swimming motility under Zn-deficient conditions, as revealed by the fact that the polar flagellar-related genes were not downregulated in the mutant. Moreover, VP_RS01470deletion produced no noticeable impact on the swarming motility and virulence in mice. qRT-PCR analysis and β-galactosidase activity assays indicated that Zur negatively regulates VP_RS01470expression in V. parahaemolyticus. Collectively, our findings suggest that ZrgA is required for Zn acquisition in V. parahaemolyticusand highlight the importance of detecting the expression of flagellar genes during analysis of motility of a mutant deficient in growth.

ABSTRACTStreptococcus suisis a major swine and zoonotic pathogen that causes severe infections. Previously, we identified 2 Spx regulators in S. suis, and demonstrated that SpxA1 affects oxidative stress tolerance and virulence. However, the mechanism behind SpxA1 function remains unclear. In this study, we targeted 4 genes that were expressed at significantly reduced levels in the spxA1mutant, to determine their specific roles in adaptation to oxidative stress and virulence potential. The Δnoxstrain exhibited impaired growth under oxidative stress conditions, suggesting that NADH oxidase is involved in oxidative stress tolerance. Using murine and pig infection models, we demonstrate for the first time that NADH oxidase is required for virulence in S. suis2. Furthermore, the enzymatic activity of NADH oxidase has a key role in oxidative stress tolerance and a secondary role in virulence. Collectively, our findings reveal that NADH oxidase plays an important part in SpxA1 function and provide a new insight into the pathogenesis of S. suis2.