P. cannabina pv. alisalensis (Pcal) is a causative agent of bacterial blight of crucifer including cabbage, radish, and broccoli. Importantly, Pcal can infect not only a wide range of Brassicaceae, but also green manure crops such as oat. However, Pcal virulence mechanisms have not been investigated and are not fully understood. We focused on coronatine (COR) function, which is one of the well-known P. syringae pv. tomato DC3000 virulence factors, in Pcal infection processes on both dicot and monocot plants. Cabbage and oat plants dip-inoculated with a Pcal KB211 COR mutant (ΔcmaA) exhibited reduced virulence compared to Pcal WT. Moreover, ΔcmaA failed to reopen stomata on both cabbage and oat, suggesting that COR facilitates Pcal entry through stomata into both plants. Furthermore, cabbage and oat plants syringe-infiltrated with ΔcmaA also showed reduced virulence, suggesting that COR is involved in overcoming not only stomatal-based defense, but also apoplastic defense. Indeed, defense related genes, including PR1 and PR2, were highly expressed in plants inoculated with ΔcmaA compared to Pcal WT, indicating that COR suppresses defense-related genes of both cabbage and oat. Additionally, SA accumulation increases after ΔcmaA inoculation compared to Pcal WT. Taken together, COR contributes to cause disease by suppressing stomatal-based defense and apoplastic defense in both dicot and monocot plants. This is the first study to investigate COR functions in the interaction of Pcal and different host plants (dicot and monocot plants) using genetically and biochemically defined COR deletion mutants.