<i>Pseudomonas syringae</i> pv. <i>actinidiae</i> Unique Effector HopZ5 Interacts with GF14C to Trigger Plant Immunity

The bacterial canker of kiwifruit caused by <i>Pseudomonas syringae</i> pv. <i>actinidiae</i> (<i>Psa</i>) is the most devastating disease threatening the global kiwifruit production. This pathogen delivers multiple effector proteins into plant cells to resist plant immune responses and facilitate their survival. Here, we focused on the unique effector HopZ5 in <i>Psa</i>, which previously has been reported to have virulence functions. In this study, our results showed that HopZ5 could cause macroscopic cell death and trigger a serious immune response by agroinfiltration in <i>Nicotiana benthamiana</i>, along with upregulated expression of immunity-related genes and significant accumulation of reactive oxygen species and callose. Subsequently, we confirmed that HopZ5 interacted with the phosphoserine-binding protein GF14C in both the nonhost plant <i>N. benthamiana</i> (NbGF14C) and the host plant kiwifruit (AcGF14C), and silencing of NbGF14C compromised HopZ5-mediated cell death, suggesting that GF14C plays a crucial role in the detection of HopZ5. Further studies showed that overexpression of NbGF14C both markedly reduced the infection of <i>Sclerotinia sclerotiorum</i> and <i>Phytophthora capsica</i> in <i>N. benthamiana</i>, and overexpression of AcGF14C significantly enhanced the resistance of kiwifruit against <i>Psa</i>, indicating that GF14C positively regulates plant immunity. Collectively, our results revealed that the virulence effector HopZ5 could be recognized by plants and interact with GF14C to activate plant immunity.