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A fliC flagellin mutant of Pseudomonas syringae effectorless polymutant DC3000D36E reveals novel death elicitation activity in Nicotiana benthamiana

Wei Zhang: Cornell University

<div><em>Pseudomonas syringae</em> pv. <em>tomato</em> DC3000 injects multiple effector proteins into plant cells via the type III secretion system (T3SS) to cause bacterial speck disease in <em>Arabidopsis</em>, tomato, and <em>Nicotiana benthamiana</em> (if Δ<em>hopQ1-1</em>). In <em>N. benthamiana</em>, effectorless polymutant DC3000D36E grows 4 logs less than DC3000Δ<em>hopQ1-1</em>, fails to trigger cell death, and displays <em>fliC</em> (flagellin)-dependent elicitation of a 15-h post-inoculation reactive oxygen species (ROS) burst that is associated with pattern-triggered immunity (PTI). In contrast, DC3000D36EΔ<em>fliC</em> loses ROS elicitation activity and triggers rapid cell death in <em>N. benthamiana</em>. A T3SS-deficient derivative of DC3000D36E<em>∆fliC</em> does not elicit cell death under the same conditions. These observations suggest that plant cell death may be triggered by one or more T3SS machinery components but is suppressed by flagellin-triggered PTI. AvrPtoB<sub>M3, </sub>a derivative of a key DC3000 effector that has site-specific mutations disrupting its E3 ubiquitin ligase domain and the two known domains for interacting with immunity-associated kinases, is a suppressor of effector-triggered immunity elicited by certain effectors. AvrPtoB<sub>M3 </sub>also suppresses death elicitation by DC3000D36E<em>∆fliC</em> in <em>N. benthamiana</em>. Ongoing experiments are exploring the basis for death elicitation by DC3000D36E<em>∆fliC</em> and its suppression by flagellin and AvrPtoB<sub>M3</sub> in this minimalized pathosystem that features native deployment and interplay of core interaction factors.</div>