Results and discussionRipAA induced the accumulation of hydrogen peroxide (H2O2) and genome DNA degradation in N. benthamiana, which were accompanied by a hypersensitive reaction. Simultaneously, the marker genes for salicylic acid (SA) signaling were induced and those for jasmonic acid (JA) signaling were reduced. N. benthamiana chloroplastic AtpB, the ATPase β subunit, was identified as an interactor with RipAA. The silencing of atpB in N. benthamiana resulted in the inability of RipAA to induce a hypersensitive response, a compatible interaction with GMI1000, and an enhanced sensitivity to bacterial wilt. Our data support the concept that RipAA determines host-range specificity by targeting the host chloroplastic AtpB.