A PRA-Rab trafficking machinery modulates NLR immune receptor plasma membrane microdomain anchoring and blast resistance in rice.

Nucleotide-binding leucine-rich repeat (NLR) receptors mediate pathogen effector-triggered immunity (ETI) in plants, and a subclass of NLRs are hypothesized to function at the plasma membrane (PM). However, how NLR traffic and PM delivery are regulated during immune responses remains largely unknown. The rice NLR PigmR confers broad-spectrum resistance to the blast fungus Magnaporthe oryzae.

A peptide-receptor module links cell wall integrity sensing to pattern-triggered immunity.

Plants employ cell-surface receptors to perceive non- or altered-self, including the integrity of their cell wall. Here we identify a specific ligand-receptor module responsive to cell wall damage that potentiates immunity in Arabidopsis. Disruption of cell wall integrity by inhibition of cellulose biosynthesis promotes pattern-triggered immunity transcriptionally in a manner dependent on the receptor kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2).

NLRs guard metabolism to coordinate pattern- and effector-triggered immunity.

Pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) in plants enable them to respond to pathogens by activating the production of defence metabolites that orchestrate immune responses. How the production of defence metabolites is promoted by immune receptors and coordinated with broad-spectrum resistance remains elusive. Here we identify the deubiquitinase PICI1 as an immunity hub for PTI and ETI in rice (Oryza sativa).

Ca sensor-mediated ROS scavenging suppresses rice immunity and is exploited by a fungal effector.

Plant immunity is activated upon pathogen perception and often affects growth and yield when it is constitutively active. How plants fine-tune immune homeostasis in their natural habitats remains elusive. Here, we discover a conserved immune suppression network in cereals that orchestrates immune homeostasis, centering on a Ca-sensor, RESISTANCE OF RICE TO DISEASES1 (ROD1).

Molecular Basis of Disease Resistance and Perspectives on Breeding Strategies for Resistance Improvement in Crops.

Crop diseases are major factors responsible for substantial yield losses worldwide, which affects global food security. The use of resistance (R) genes is an effective and sustainable approach to controlling crop diseases. Here, we review recent advances on R gene studies in the major crops and related wild species.

RRM Transcription Factors Interact with NLRs and Regulate Broad-Spectrum Blast Resistance in Rice.

Nucleotide-binding site leucine-rich repeat (NLR) receptors perceive pathogen effectors and trigger plant immunity. However, the mechanisms underlying NLR-triggered defense responses remain obscure. The recently discovered Pigm locus in rice encodes a cluster of NLRs, including PigmR, which confers broad-spectrum resistance to blast fungus.

A nucleotide-binding site-leucine-rich repeat receptor pair confers broad-spectrum disease resistance through physical association in rice.

Rice blast caused by Magnaporthe oryzae is the most destructive fungal disease in crops, greatly threatening rice production and food security worldwide. The identification and utilization of broad-spectrum resistance genes are considered to be the most economic and effective method to control the disease. In the past decade, many blast resistance ( R) genes have been identified, which mainly encode nucleotide-binding leucine-rich repeat (NLR) receptor family and confer limited race-specific resistance to the fungal pathogen.

Epigenetic regulation of antagonistic receptors confers rice blast resistance with yield balance.

Crop breeding aims to balance disease resistance with yield; however, single resistance (R) genes can lead to resistance breakdown, and R gene pyramiding may affect growth fitness. Here we report that the rice locus contains a cluster of genes encoding nucleotide-binding leucine-rich repeat (NLR) receptors that confer durable resistance to the fungus without yield penalty. Among these NLR receptors, PigmR confers broad-spectrum resistance, whereas PigmS competitively attenuates PigmR homodimerization to suppress resistance.

An E3 Ubiquitin Ligase-BAG Protein Module Controls Plant Innate Immunity and Broad-Spectrum Disease Resistance.

Programmed cell death (PCD) and immunity in plants are tightly controlled to promote antimicrobial defense while preventing autoimmunity. However, the mechanisms contributing to this immune homeostasis are poorly understood. Here, we isolated a rice mutant ebr1 (enhanced blight and blast resistance 1) that shows enhanced broad-spectrum bacterial and fungal disease resistance, but displays spontaneous PCD, autoimmunity, and stunted growth.