Abstract
Extensive research revealed tremendous details about how plants sense pathogen effectors during effector-triggered immunity (ETI). However, less is known about downstream signaling events. In this report, we demonstrate that prolonged activation of MPK3 and MPK6, two Arabidopsis pathogen-responsive mitogen-activated protein kinases (MPKs), is essential to ETI mediated by both coiled coil-nucleotide binding site-leucine rich repeats (CNLs) and toll/interleukin-1 receptor nucleotide binding site-leucine rich repeats (TNLs) types of R proteins. MPK3/MPK6 activation rapidly alters the expression of photosynthesis-related genes and inhibits photosynthesis, which promotes the accumulation of superoxide () and hydrogen peroxide (H2O2), two major reactive oxygen species (ROS), in chloroplasts under light. In the chemical-genetically rescued mpk3 mpk6 double mutants, ETI-induced photosynthetic inhibition and chloroplastic ROS accumulation are compromised, which correlates with delayed hypersensitive response (HR) cell death and compromised resistance. Furthermore, protection of chloroplasts by expressing a plastid-targeted cyanobacterial flavodoxin (pFLD) delays photosynthetic inhibition and compromises ETI. Collectively, this study highlights a critical role of MPK3/MPK6 in manipulating plant photosynthetic activities to promote ROS accumulation in chloroplasts and HR cell death, which contributes to the robustness of ETI. Furthermore, the dual functionality of MPK3/MPK6 cascade in promoting defense and inhibiting photosynthesis potentially allow it to orchestrate the trade-off between plant growth and defense in plant immunity.
Highlights
Plant defense against invading pathogens relies on a two-layered innate immune system
One of the responses observed is the inhibition of photosynthesis and the global down-regulation of genes that regulate this process, similar to what is frequently observed in plants under various biotic stress conditions
It is unclear whether the inhibition is a passive response caused by stresses/ pathogens or a response actively regulated by host signaling pathways, and if so, what the outcomes/functions are of such active inhibition
Summary
Plant defense against invading pathogens relies on a two-layered innate immune system. The first is the sensing of pathogen/microbe-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs), which induces a basal level resistance known as PAMP-triggered immunity (PTI) [1,2,3,4,5]. The second line of plant defense is activated by plant resistance (R) protein-mediated detection of pathogenic effectors, known as effector-triggered immunity (ETI). The majority of plant R proteins are nucleotide-binding site leucine-rich repeat (NBS-LRR) proteins, having a central NBS-ARC domain (ARC: Apaf, R proteins, and CED-4) and a C-terminal leucine-rich repeat (LRR) domain [14,15,16,17] Based on their N-terminal domains, plant NBS-LRR R proteins (NLRs) are classified into two families, the coiled coil-nucleotide binding site-leucine rich repeat (CNL) family and the Toll/interleukin-1 receptor-nucleotide binding site-leucine rich repeat (TNL) family [14,15,16,17]. NLRs recognize their cognate effectors by direct protein–protein interactions, while the indirect recognition describes mechanisms by which NLRs sense effectors by monitoring modified self, including the “guard,” the “decoy,” and the “integrated decoy” model [18,19,20]
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