Plant Innate Immunity Mechanisms in Rice

Rice employs a two-tiered defence system to detect and resist pathogenic attack. The first tier, pattern-triggered immunity (PTI), is initiated by cell-surface pattern-recognition receptors (PRRs) that perceive conserved microbial signatures and activate downstream signalling cascades, including calcium influx, mitogen-activated protein kinase (MAPK) modules and generation of reactive oxygen species (ROS). To overcome PTI, adapted pathogens deliver effector proteins that suppress these early defences. The second tier, effector-triggered immunity (ETI), is mediated by intracellular nucleotide-binding leucine-rich repeat (NLR) receptors that recognise effectors directly or indirectly, leading to amplified defence gene expression and, frequently, a hypersensitive response. Precise modulation of immune activation is achieved through post-translational modifications such as phosphorylation and ubiquitination, which regulate receptor abundance, signal transduction and hormone cross-talk. Recent discoveries have unveiled how fungal effectors reprogramme host transcription, manipulate ion channels and mimic host regulators to dampen immunity, while natural variation in key components offers avenues for breeding resilient rice cultivars without compromising yield.

Research from Nature Portfolio

Studies have uncovered that the rice blast fungus secretes the effector MoSPAB1, which binds directly to the promoter of the rice Bsr-d1 gene, inducing its expression and thereby subverting immunity. This interaction hinges on a conserved peptide motif within MoSPAB1 and competes with the rice transcription factor MYBS1 for promoter occupancy. Homologues of MoSPAB1 in diverse fungal species suggest that transcriptional activation of host defence suppressors is a widespread virulence strategy.

Plant Innate Immunity Mechanisms in Rice publication trend

The graph below shows the total number of articles in plant innate immunity mechanisms in rice across all publications each year (not limited to Nature Index journals).

Technical terms

Pattern-triggered immunity (PTI): The basal defence response activated by PRRs upon detection of conserved microbial molecules.

Effector-triggered immunity (ETI): A robust immune response elicited by intracellular NLR receptors recognising pathogen effectors.

Pattern-recognition receptor (PRR): A membrane-bound sensor that detects pathogen-associated molecular patterns to initiate PTI.

Nucleotide-binding leucine-rich repeat (NLR) receptor: An intracellular immune receptor that activates ETI upon effector recognition.

Reactive oxygen species (ROS): Highly reactive molecules produced during immune activation that can directly inhibit pathogens and signal defence pathways.

Ubiquitination: A reversible post-translational modification attaching ubiquitin to proteins, regulating their stability, localisation or activity.

References

1. Magnaporthe oryzae effector MoSPAB1 directly activates rice Bsr-d1 expression to facilitate pathogenesis. Nature Communications (2023).
2. Ca2+ sensor-mediated ROS scavenging suppresses rice immunity and is exploited by a fungal effector. Cell (2021).
3. The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel. PLOS Pathogens (2018).
4. Proteomic Analysis of Ubiquitinated Proteins in Rice (Oryza sativa) After Treatment With Pathogen-Associated Molecular Pattern (PAMP) Elicitors. Frontiers in Plant Science (2018).