Abstract
Plant pathogens deliver effectors to alter host processes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. 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. Pi04314 interacts with three host protein phosphatase 1 catalytic (PP1c) isoforms, causing their re-localization from the nucleolus to the nucleoplasm. Re-localization of PP1c-1 also occurs during infection and is dependent on an R/KVxF motif in the effector. Silencing the PP1c isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating that host PP1c activity is required for disease. Moreover, expression of PP1c–1mut abolishes enhanced leaf colonization mediated by in planta Pi04314 expression. We argue that PP1c isoforms are susceptibility factors forming holoenzymes with Pi04314 to promote late blight disease.
Highlights
Plant pathogens deliver effectors to alter host processes
Three RXLR effectors from P. infestans have been shown to suppress pattern-triggered immunity (PTI) mediated by the bacterial pathogen-associated molecular pattern (PAMP) flg[22] by preventing mitogenactivated protein kinase (MAPK) phosphorylation and activation[19], and a further P. infestans RXLR effector, PexRD2, interacts with the kinase domain of MAP3Ke to prevent signal transduction leading to cell death mediated by the receptor Cf4
To evaluate whether Pi04314 plays a role in contributing to P. infestans virulence, green fluorescent protein (GFP)–Pi04314 was transiently expressed in one-half of an N. benthamiana leaf with free GFP expressed in the other
Summary
Plant pathogens deliver effectors to alter host processes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. 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. Three RXLR effectors from P. infestans have been shown to suppress PTI mediated by the bacterial PAMP flg[22] by preventing mitogenactivated protein kinase (MAPK) phosphorylation and activation[19], and a further P. infestans RXLR effector, PexRD2, interacts with the kinase domain of MAP3Ke to prevent signal transduction leading to cell death mediated by the receptor Cf4 These examples demonstrate that oomycetes can either directly suppress PTI by altering PTMs that positively regulate immunity, or, in the case of HaRxL44, can promote ubiquitination of an immune regulator to affect its degradation
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