PdeK/PdeR, the two-component system (TCS), was previously shown to regulate the virulence of the rice bacterial blight pathogen <i>Xanthomonas oryzae </i>pv. <i>oryzae </i>(Xoo). The response regulator PdeR harbors phosphodiesterase (PDE) activity to degrade bacterial second messenger cyclic di-GMP. To understand the downstream signaling pathway mediated by PdeR, we started with looking for its interacting partners in Xoo strain PXO99^A. Here, we identified a response regulator PXO_04421, named as TriP, as an interactor of PdeR. Yeast two-hybrid (Y2H) and GST pull-down assays confirmed the PdeR-Trip interaction. Interestingly, the interaction was inhibited by high concentration of c-di-GMP. Virulence assays demonstrated that the <i>triP </i>mutant caused shorter lesion length on rice leaves than the wild type, and its ability to progress through the xylem tissue was also impaired. Moreover, both the <i>pdeR </i>and the <i>triP </i>single mutant produced less exopolysaccharide (EPS), while the <i>pdeR/triP </i>double mutant produced similar level of EPS with that of the <i>triP </i>mutant. These results indicated that TriP and PdeR are functionally related in regulation of bacterial virulence. Additionally, RNA-seq analysis revealed a considerable overlap in the up-regulated genes in the two single mutants, which further implied that TriP might mediate a part of the PdeR-mediated signaling in Xoo.