A Ralstonia solanacearum effector regulates plant cell death by disrupting the homeostasis of the BPA1-ACD11 complex

Effectors secreted by phytopathogenic bacteria can suppress ETI responses induced by avirulence effectors, thereby overcoming crop resistance. However, the detailed mechanisms remain largely unknown. We report that the effector RipD from Ralstonia solanacearum regulates plant cell death in a protein abundance-dependent manner. RipD targets Arabidopsis BPA1, which directly interacts with the key cell death negative regulator ACD11. RipD competes with ACD11 for binding to BPA1, leading to the selective degradation of BPA1 via autophagy, sparing ACD11. A lower dose of RipD promotes BPA1 degradation but leads to ACD11 accumulation, thereby inhibiting RipAA-induced cell death. Conversely, higher levels of RipD degrade both BPA1 and ACD11, resulting in autophagy-dependent cell death. Visualization of RipD delivery by R. solanacearum indicated that it reaches levels sufficient to promote ACD11 accumulation and inhibit cell death. Our study reveals a novel mechanism by which an effector inhibits ETI and, for the first time, highlights the critical role of protein abundance in its function.