Global regulator DksA modulates virulence of .

DksA with (p)ppGpp regulates a wide range of gene transcriptions during the stringent response. The aim of this study was to identify a DksA ortholog in and clarify the roles of DksA in bacterial physiology and virulence. The ∆ mutant and its complemented strains were constructed using ATCC 17978. The in ATCC 17978 was identified to using sequence homology, protein structure prediction, and gene expression patterns under different culture conditions. The ∆ mutant strain showed a filamentous morphology compared with the wild-type (WT) strain. Bacterial growth was decreased in the ∆ mutant strain under static conditions. Surface motility was decreased in the ∆ mutant strain compared with the WT strain. In contrast, biofilm formation was increased and biofilm-associated genes, such as and , were upregulated in the ∆ mutant strain. The ∆ mutant strain produced less autoinducers than the WT strain. The expression of and was significantly decreased in the ∆ mutant strain. Furthermore, the ∆ mutant strain showed less bacterial burden and milder histopathological changes in the lungs of mice than the WT strain. Mice survival was also significantly different between the ∆ mutant and WT strains. Conclusively, DksA is directly or indirectly involved in regulating a wide range of genes associated with bacterial physiology and virulence, which contributes to the pathogenesis of . Thus, DksA is a potential anti-virulence target for infection.