Among the strategies employed by pathogens to suppress PTI is the secretion of effectors that act either in the apoplast or are delivered inside living plant cells to target regulatory host proteins. Host-adapted pathogens have evolved to manipulate processes in plants that result in suppression of PTI 2. Similar content being viewed by othersĭetection of conserved microbial molecules (microbe-associated molecular patterns) or the products generated by microbial degradation of host cell walls (damage-associated molecular patters) at the plasma membrane by plant pattern recognition receptors, leads to pattern-triggered immunity (PTI) 1. We argue that PP1c isoforms are susceptibility factors forming holoenzymes with Pi04314 to promote late blight disease. Moreover, expression of PP1c–1mut abolishes enhanced leaf colonization mediated by in planta Pi04314 expression. Silencing the PP1c isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating that host PP1c activity is required for disease. Re-localization of PP1c-1 also occurs during infection and is dependent on an R/KVxF motif in the effector. Pi04314 interacts with three host protein phosphatase 1 catalytic (PP1c) isoforms, causing their re-localization from the nucleolus to the nucleoplasm. Here, we show that in planta expression of the RXLR effector Pi04314 enhances leaf colonization by Phytophthora infestans via activity in the host nucleus and attenuates induction of jasmonic and salicylic acid-responsive genes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. Plant pathogens deliver effectors to alter host processes.
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