ZrgA contributes to zinc acquisition in Vibrio parahaemolyticus.

Metals are nutrients essential for almost all lifeforms. Bacteria have evolved several mechanisms to overcome the metal restrictions imposed by the host. causes 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 to of encodes the putative Zn transporter ZrgABCDE, whose homologs are widely distributed in . RNA sequencing analysis revealed that modulates 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 () deletion exhibited impaired growth under Zn-deficient conditions, indicating that plays the predominant role in Zn acquisition. The deletion 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, deletion 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 expression in . Collectively, our findings suggest that ZrgA is required for Zn acquisition in and highlight the importance of detecting the expression of flagellar genes during analysis of motility of a mutant deficient in growth.