The <i>Pseudomonas syringae</i> Type III Effector HopF2 Suppresses Arabidopsis Stomatal Immunity

Pseudomonas syringae subverts plant immune signalling through injection of type III secreted effectors (T3SE) into host cells. The T3SE HopF2 can disable Arabidopsis immunity through Its ADP-ribosyltransferase activity. Proteomic analysis of HopF2 interacting proteins identified a protein complex containing ATPases required for regulating stomatal aperture, suggesting HopF2 may manipulate stomatal immunity. Here we report HopF2 can inhibit stomatal immunity independent of its ADP-ribosyltransferase activity. Transgenic expression of HopF2 in Arabidopsis inhibits stomatal closing in response to P. syringae and increases the virulence of surface inoculated P. syringae. Further, transgenic expression of HopF2 inhibits flg22 induced reactive oxygen species production. Intriguingly, ADP-ribosyltransferase activity is dispensable for inhibiting stomatal immunity and flg22 induced reactive oxygen species. Together, this implies HopF2 may be a bifunctional T3SE with ADP-ribosyltransferase activity required for inhibiting apoplastic immunity and an independent function required to inhibit stomatal immunity.丁香假单胞菌（Pseudomonas syringae）通过向宿主细胞注射III型分泌效应蛋白（type III secreted effectors，T3SE）以破坏植物的免疫信号转导通路。III型分泌效应蛋白HopF2可通过其ADP核糖基转移酶（ADP-ribosyltransferase）活性抑制拟南芥（Arabidopsis）的免疫反应。研究人员通过对HopF2互作蛋白进行蛋白质组学分析，鉴定得到一个包含调控气孔开度必需ATP酶的蛋白复合物，这提示HopF2或可操控气孔免疫。本研究证实，HopF2可独立于其ADP核糖基转移酶活性抑制气孔免疫。在拟南芥中转基因表达HopF2，可抑制其针对丁香假单胞菌的气孔关闭反应，并提升表面接种的丁香假单胞菌的毒力。进一步实验表明，转基因表达HopF2还可抑制flg22诱导的活性氧（reactive oxygen species）产生。值得注意的是，ADP核糖基转移酶活性并非HopF2抑制气孔免疫及flg22诱导活性氧产生所必需。综上，上述结果表明HopF2是一种双功能III型分泌效应蛋白：其ADP核糖基转移酶活性负责抑制质外体免疫，而另一独立功能则用于抑制气孔免疫。