Interplay between cell-surface receptor and intracellular NLR-mediated immune responses.

The functional link between cell-surface receptors and intracellular NLR immune receptors is a critical aspect of plant immunity. To establish disease, successful pathogens have evolved mechanisms to suppress cell-surface immune signalling. In response, plants have adapted by evolving NLRs that recognize pathogen effectors involved in this suppression, thereby counteracting their immune-suppressing function. This ongoing co-evolutionary struggle has seemingly resulted in intertwined signalling pathways in some plant species, where NLRs form a separate signalling branch downstream of activated cell-surface receptor complexes essential for full immunity. Understanding these interconnected receptor networks could lead to novel strategies for developing durable disease resistance.

A novel module regulating ROS in NLR-mediated immunity.

The regulatory mechanisms of apoplastic reactive oxygen species (ROS) production during pattern-triggered immunity (PTI) are well known. However, how ROS levels are regulated during effector-triggered immunity (ETI) remains largely unknown. Recently, Zhang et al. discovered that MAPK-Alfin-like 7 module enhances nucleotide-binding, leucine-rich repeat receptor (NLR)-mediated immunity by negatively regulating genes encoding ROS scavenging enzymes, deepening our understanding of ROS control during ETI in plants.

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. Here, we identify PIBP1 (PigmR-INTERACTING and BLAST RESISTANCE PROTEIN 1), an RRM (RNA-recognition motif) protein that specifically interacts with PigmR and other similar NLRs to trigger blast resistance. PigmR-promoted nuclear accumulation of PIBP1 ensures full blast resistance. We find that PIBP1 and a homolog, Os06 g02240, bind DNA and function as unconventional transcription factors at the promoters of the defense genes OsWAK14 and OsPAL1, activating their expression. Knockout of PIBP1 and Os06 g02240 greatly attenuated blast resistance. Collectively, our study discovers previously unappreciated RRM transcription factors that directly interact with NLRs to activate plant defense, establishing a direct link between transcriptional activation of immune responses with NLR-mediated pathogen perception.