Nuclear Localization of HopA1(Pss61) Is Required for Effector-Triggered Immunity

Abstract

Plant resistance proteins recognize cognate pathogen avirulence proteins (also named effectors) to implement the innate immune responses called effector-triggered immunity. Previously, we reported that hopA1 from Pseudomonas syringae pv. syringae strain 61 was identified as an avr gene for Arabidopsis thaliana. Using a forward genetic screen approach, we cloned a hopA1-specific TIR-NBS-LRR class disease resistance gene, RESISTANCE TO PSEUDOMONAS SYRINGAE6 (RPS6). Many resistance proteins indirectly recognize effectors, and RPS6 is thought to interact with HopA1(Pss61) indirectly by surveillance of an effector target. However, the involved target protein is currently unknown. Here, we show RPS6 is the only R protein that recognizes HopA1(Pss61) in Arabidopsis wild-type Col-0 accession. Both RPS6 and HopA1(Pss61) are co-localized to the nucleus and cytoplasm. HopA1(Pss61) is also distributed in plasma membrane and plasmodesmata. Interestingly, nuclear localization of HopA1(Pss61) is required to induce cell death as NES-HopA1(Pss61) suppresses the level of cell death in Nicotiana benthamiana. In addition, in planta expression of hopA1(Pss61) led to defense responses, such as a dwarf morphology, a cell death response, inhibition of bacterial growth, and increased accumulation of defense marker proteins in transgenic Arabidopsis. Functional characterization of HopA1(Pss61) and RPS6 will provide an important piece of the ETI puzzle.