High Humidity or Addition of ABA Compensates for dspEF Deletion Mutation in Pectobacterium carotovorum

Pectobacterium carotovorum is a gram-negative phytopathogenic bacterium that causes soft rot disease on diverse plant species. It encodes the type III secretion system effector protein, DspE, and its chaperone, DspF. The DspE family proteins form water and solute channels in plant cells, flooding the apoplast to aid bacterial multiplication. In Pseudomonas syringae, the DspE ortholog, AvrE, upregulates abscisic acid (ABA) expression, leading to stomatal closure. In this study, a P. carotovorum dspEF mutant did not cause leaf cell death in tobacco leaves. This observation is supported by the lower expression of plant cell wall–degrading enzymes such as pelB, pelI, celV, prtW, and the quorum-sensing system transcript expI in tobacco plants prior to visual symptoms (5 h postinoculation). Interestingly, neither dspE/F nor hrpL mutation affected synthesis of quorum-sensing signaling molecule acyl-homoserine lactone under microbiological settings. However, maceration symptoms occurred if leaves infiltrated with the dspEF mutant were kept under high humidity or detached postinfiltration. These leaves showed elevated transcription of ABA synthesis genes compared with infiltrated leaves maintained on the plant under ambient conditions. To validate this involvement, coinfiltration of ABA with the dspEF mutant restored its ability to cause maceration in attached leaves under ambient conditions. Overall, our data suggest that DspE/F facilitates host susceptibility by creating an aqueous apoplast, promoting ABA accumulation and stomata closure.