Pathogen effector-associated nuclear-localization of RPW8.2 amplifies its expression to boost immunity in Arabidopsis

Author:

Zhao Jing-haoORCID,Huang Yan-yan,Wang He,Yang Xue-meiORCID,Fan Jing,Li Yan,Pu Mei,Zhou Shi-xin,Zhang Ji-wei,Zhao Zhi-xue,Li Guo-bang,Hassan Beenish,Hu Xiao-hong,Chen Xue-wei,Xiao ShunyuanORCID,Wu Xian-jun,Wang Wen-mingORCID

Abstract

AbstractRESISTANCE TO POWDERY MILDEW 8 (RPW8) defines a unique N-terminal coiled-coil domain of nucleotide-binding and leucine-rich repeat immune receptors required for immune signaling in plants. Arabidopsis RPW8.2 is specifically induced by the powdery mildew (PM) fungus (Golovinomyces cichoracearum) in the infected epidermal cells to activate immunity. The mechanism of RPW8.2-induction is not well understood. Here, we identify aG. cichoracearumfactor delivered to the nucleus of the host cell, named Gc-RPW8.2 interacting protein 1 (GcR8IP1). Ectopic expression of GcR8IP1 in Arabidopsis orNicotiana benthamianasuppressed host immune responses and enhanced susceptibility to PM. Host-induced gene silencing ofGcR8IP1compromised PM infectivity in susceptible Arabidopsis plants. Co-expression of GcR8IP1 with RPW8.2 increased nuclear localization of RPW8.2, which in turn, promoted transcriptional amplification ofRPW8.2. Thus, RPW8.2-dependent defense strengthening is due to altered partitioning of RPW8.2 by an effector of a PM fungus, which exemplifies an atypical form of effector-triggered immunity.

Publisher

Cold Spring Harbor Laboratory

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