| Summary: | The type VI secretion system (T6SS) is a large secretory device, widely found in Gram-negative bacteria, which plays important roles in virulence, bacterial competition, and environmental adaptation. <i>Vibrio alginolyticus</i> (<i>V. alginolyticus</i>) is an opportunistic pathogen that causes vibriosis in aquaculture animals. <i>V. alginolyticus</i> possesses two type VI secretion systems (named the T6SS1 and T6SS2), but their functions remain largely unclear. In this paper, the roles of the core component of the T6SS2 cluster of <i>V. alginolyticus</i> HY9901, hemolysin-coregulated protein2 coding gene <i>hcp2</i>, are reported. Deletion of <i>hcp2</i> clearly impaired the swarming motility, adhesive capacity, and pathogenicity of <i>V. alginolyticus</i> against zebrafish. Furthermore, transmission electron microscopy (TEM) found that the abnormal morphology of flagellum filament in the <i>hcp2</i> mutant strain could be partially restored by <i>hcp2</i> complementarity. By proteomic and RT-qPCR analysis, we confirmed that the expression levels of flagellar flagellin and assembly-associated proteins were remarkably decreased in an <i>hcp2</i> mutant strain, compared with the wild-type strain, and could be partially restored with a supply of <i>hcp2</i>. Accordingly, <i>hcp2</i> had a positive influence on the transcription of flagellar regulons <i>rpoN</i>, <i>rpoS</i>, and <i>fliA</i>; this was verified by RT-qPCR. Taken together, these results suggested that <i>hcp2</i> was involved in mediating the motility, adhesion, and pathogenicity of <i>Vibrio alginolyticus</i> through positively impacting its flagellar system.
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