How activated NLRs induce anti-microbial defenses in plants.

Farid El Kasmi

doi:10.1042/bst20210242

Abstract

Plants utilize cell-surface localized and intracellular leucine-rich repeat (LRR) immune receptors to detect pathogens and to activate defense responses, including transcriptional reprogramming and the initiation of a form of programmed cell death of infected cells. Cell death initiation is mainly associated with the activation of nucleotide-binding LRR receptors (NLRs). NLRs recognize the presence or cellular activity of pathogen-derived virulence proteins, so-called effectors. Effector-dependent NLR activation leads to the formation of higher order oligomeric complexes, termed resistosomes. Resistosomes can either form potential calcium-permeable cation channels at cellular membranes and initiate calcium influxes resulting in activation of immunity and cell death or function as NADases whose activity is needed for the activation of downstream immune signaling components, depending on the N-terminal domain of the NLR protein. In this mini-review, the current knowledge on the mechanisms of NLR-mediated cell death and resistance pathways during plant immunity is discussed.

Highlights

Beside physical barriers, including bark, leaf hairs, waxy cuticles and plant cell walls, plant-invadingorganisms have to face a highly sophisticated and heavily interconnected twotiered, receptor based innate immune system [1]
It is possible that the calcium influx activates other cation channels important for immunity and components required for cell collapse, and that damage-associated molecular patterns (DAMPs) might be released by the nucleotide-binding LRR receptors (NLRs) formed pores to create signals enhancing immune responses that may lead to systemic resistance and maybe cell death
It is very likely that NRG1.1/ NRG1A oligomerizes and forms high molecular weight complexes in an activation dependent manner — similar to ZAR1- as an NRG1.1/NRG1A P-loop loss-of-function mutant, affected in nucleotide binding, did not. Based on these recent findings and the fact that NLR-triggered effector-triggered immunity (ETI) leads to prolonged calcium influxes, conceivably, all CNL and require helper NLR (RNL) triggered cell death responses may require the formation of some kind of channel, most likely cation channels, in cellular membranes

Summary

Introduction

Beside physical barriers, including bark, leaf hairs (trichomes), waxy cuticles and plant cell walls, plant-invading (micro-)organisms have to face a highly sophisticated and heavily interconnected twotiered, receptor based innate immune system [1]. It is possible that the calcium influx activates other cation channels important for immunity (for example the CNGCs) and components required for cell collapse, and that damage-associated molecular patterns (DAMPs) might be released by the NLR formed pores to create signals enhancing immune responses that may lead to systemic resistance and maybe cell death.

Results

Conclusion