Activation and Regulation of NLR Immune Receptor Networks
- PMID: 35941738
- DOI: 10.1093/pcp/pcac116
Activation and Regulation of NLR Immune Receptor Networks
Abstract
Plants have many types of immune receptors that recognize diverse pathogen molecules and activate the innate immune system. The intracellular immune receptor family of nucleotide-binding domain leucine-rich repeat-containing proteins (NLRs) perceives translocated pathogen effector proteins and executes a robust immune response, including programmed cell death. Many plant NLRs have functionally specialized to sense pathogen effectors (sensor NLRs) or to execute immune signaling (helper NLRs). Sub-functionalized NLRs form a network-type receptor system known as the NLR network. In this review, we highlight the concept of NLR networks, discussing how they are formed, activated and regulated. Two main types of NLR networks have been described in plants: the ACTIVATED DISEASE RESISTANCE 1/N REQUIREMENT GENE 1 network and the NLR-REQUIRED FOR CELL DEATH network. In both networks, multiple helper NLRs function as signaling hubs for sensor NLRs and cell-surface-localized immune receptors. Additionally, the networks are regulated at the transcriptional and posttranscriptional levels, and are also modulated by other host proteins to ensure proper network activation and prevent autoimmunity. Plant pathogens in turn have converged on suppressing NLR networks, thereby facilitating infection and disease. Understanding the NLR immune system at the network level could inform future breeding programs by highlighting the appropriate genetic combinations of immunoreceptors to use while avoiding deleterious autoimmunity and suppression by pathogens.
Keywords: Autoimmunity; Host–pathogen interaction; Immune receptor network; NLR integrated domain; Nucleotide-binding domain and leucine-rich-repeat-containing protein; Pathogen effector.
© The Author(s) 2022. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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