Abstract
The induction of rapid cell death is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. However, activation of cell death comes at a high cost, as dead cells will no longer be available for defense responses nor general metabolic processes. In addition, necrotrophic pathogens that thrive on dead tissue, take advantage of cell death-triggering mechanisms. Mechanisms by which plants solve this conundrum remain described. Here, we identify PLANT SMY2-TYPE ILE-GYF DOMAIN-CONTAINING PROTEIN 1 (PSIG1) and show that PSIG1 helps to restrict cell death induction during pathogen infection. Inactivation of PSIG1 does not result in spontaneous lesions, and enhanced cell death in psig1 mutants is independent of salicylic acid (SA) biosynthesis or reactive oxygen species (ROS) production. Moreover, PSIG1 interacts with SMG7, which plays a role in nonsense-mediated RNA decay (NMD), and the smg7-4 mutant allele mimics the cell death phenotype of the psig1 mutants. Intriguingly, the psig1 mutants display enhanced susceptibility to the hemi-biotrophic bacterial pathogen. These findings point to the existence and importance of the SA- and ROS-independent cell death constraining mechanism as a part of the plant immune system.
Highlights
Programmed cell death (PCD) has crucial roles in development and immunity in multicellular organisms [1]
Cell death induction can backfire on plants because of the diversified infection strategies of plant pathogens
Our findings suggest that the restriction of cell death can have benefits for plants to defend themselves against hemibiotrophic bacterial pathogen infections
Summary
Programmed cell death (PCD) has crucial roles in development and immunity in multicellular organisms [1]. ETI is primarily effective against biotrophic and hemi-biotrophic pathogens [2], which obtain nutrients from live host cells and actively suppress the first layer of the plant immune system, pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). The contribution of HR cell death to resistance against hemi-biotrophic pathogens, which switch from a biotrophic phase to a necrotrophic one [4], is still under debate [5,6,7]. Under this premise, minimizing the induction of cell death, as part of a defense response, would result in an advantage for plants against pathogens that can benefit from dead cells
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