Homologous Effectors of Pseudomonas syringae pv. actinidiae HopBB1-1/HopBB1-2 Interact with DRT100 to Trigger Plant Immunity

Bacterial effectors are considered potent weapons deployed into plant cells to suppress host immunity. Pseudomonas syringae pv. actinidiae (Psa), the causal agent of kiwifruit bacterial canker, is a devastating pathogen posing a global threat to kiwifruit production. Although Psa delivers multiple effectors into plant cells, the molecular mechanisms governing effector-mediated susceptibility remain poorly understood. Here, we report that HopBB1-1 and HopBB1-2, the sole pair of homologous proteins in PsaM228, function redundantly in virulence. Whereas deletion of either effector individually did not affect bacterial pathogenicity, simultaneous deletion of both significantly reduced bacterial growth in planta. Both effectors can induce cell death and activate a series of immune response individually in Nicotiana benthamiana, and we further found that HopBB1-1 and HopBB1-2 both interacted with a plant protein, DNA damage repair and tolerance, DRT100, in both nonhost and host plants. Overexpression of AcDRT100 enhanced the kiwifruit resistance to Psa, underscoring its positive role in plant immunity and potential as a candidate gene for breeding resistant cultivars. Crucially, the virulence function of HopBB1-1/HopBB1-2 depends on AcDRT100, and NbDRT100 is required for HopBB1-1/HopBB1-2-induced cell death in N. benthamiana, indicating that DRT100 acts as a common target in both plants. Our findings uncover a sophisticated and precise effector-target module in Psa pathogenesis, revealing how redundant virulence functions are directed at a key regulator of host immunity, DRT100, which we identify as a promising candidate for developing disease-resistant varieties.