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This study shows that the expression of  yjcC , an in vivo expression (IVE) gene, and the stress response regulatory genes  soxR ,  soxS , and  rpoS  are paraquat inducible in  Klebsiella pneumoniae  CG43. The deletion of  rpoS  or  soxRS  decreased  yjcC  expression, implying an RpoS- or SoxRS-dependent control. After paraquat or H 2 O 2  treatment, the deletion of  yjcC  reduced bacterial survival. These effects could be complemented by introducing the Δ yjcC  mutant with the YjcC-expression plasmid pJR1. The recombinant protein containing only the YjcC-EAL domain exhibited phosphodiesterase (PDE) activity; overexpression of  yjcC  has lower levels of cyclic di-GMP. The  yjcC  deletion mutant also exhibited increased reactive oxygen species (ROS) formation, oxidation damage, and oxidative stress scavenging activity. In addition, the  yjcC  deletion reduced capsular polysaccharide production in the bacteria, but increased the LD50 in mice, biofilm formation, and type 3 fimbriae major pilin MrkA production. Finally, a comparative transcriptome analysis showed 34 upregulated and 29 downregulated genes with the increased production of YjcC. The activated gene products include glutaredoxin I, thioredoxin, heat shock proteins, chaperone, and MrkHI, and proteins for energy metabolism (transporters, cell surface structure, and transcriptional regulation). In conclusion, the results of this study suggest that YjcC positively regulates the oxidative stress response and mouse virulence but negatively affects the biofilm formation and type 3 fimbriae expression by altering the c-di-GMP levels after receiving oxidative stress signaling inputs.

YjcC, a c-di-GMP Phosphodiesterase Protein, Regulates the Oxidative Stress Response and Virulence of Klebsiella pneumoniae CG43