The first line of defence is mounted by pattern recognition receptors, or PRRs, which sit at the cell surface and detect conserved microbial molecules known as microbe-associated molecular patterns. These include bacterial flagellin, the translation factor EF-Tu, fungal chitin and bacterial peptidoglycan. When a PRR such as the flagellin receptor FLS2 binds its ligand, it recruits a co-receptor kinase called BAK1, forming an active receptor complex that triggers a cascade of phosphorylation events. Structural studies over the past decade have revealed the atomic details of these interactions, showing how ligand binding induces dimerization and allosteric activation of the kinase domains. The review emphasizes that receptor-like proteins, which lack an intracellular kinase domain, rely on partner kinases such as SOBIR1 and BAK1 to transduce signals, and that recent work has clarified how these complexes assemble and activate downstream pathways.

Once a PRR is activated, a receptor-like cytoplasmic kinase called BIK1 is released from the receptor complex and phosphorylates a remarkable range of targets. BIK1 directly activates the NADPH oxidase RbohD, driving a burst of reactive oxygen species that reinforces cell walls and signals to neighbouring cells. It also regulates calcium channels, including CNGCs and OSCA1.3, allowing cytosolic calcium concentrations to rise rapidly. This calcium influx is not merely a byproduct; it is a central hub of immune signalling. Calcium-dependent protein kinases decode the calcium signature and phosphorylate transcription factors and metabolic enzymes, while calcium-activated metacaspases release immunomodulatory peptides from damaged cells. The review highlights how this spatiotemporally controlled calcium symphony, as one group of researchers has described it, links pattern recognition to gene expression, stomatal closure and the production of antimicrobial compounds.

The second branch of plant immunity operates inside the cell. Intracellular nucleotide-binding leucine-rich repeat receptors, or NLRs, detect pathogen effectors, the virulence proteins that pathogens inject into host cells to suppress pattern-triggered immunity. The gene-for-gene concept, articulated by Harold Flor in the 1970s, predicted that for every resistance gene in the plant there is a corresponding avirulence gene in the pathogen. Decades of work have vindicated this idea at the molecular level. Some NLRs directly bind effectors, while others act as guards or decoys, monitoring host proteins that effectors modify. Integrated domains, which are fusions of host target mimics into the NLR architecture, allow single receptors to sense effectors that manipulate specific host processes. The review traces this conceptual evolution from the cloning of the first NLR genes in the 1990s to the recent explosion of structural biology that has revealed how these receptors work.

The most striking recent discovery in this field concerns resistosomes. When certain NLRs recognize their cognate effectors, they do not simply change shape; they oligomerize into large, ordered complexes that function as channels or enzymes. The ZAR1 resistosome, for example, forms a pentameric calcium-permeable channel in the plasma membrane, flooding the cytosol with calcium and triggering cell death at the infection site. Helper NLRs of the NRC and ADR1 families form hexameric resistosomes with similar channel activity, while TIR-domain-containing NLRs act as NAD-cleaving enzymes that produce small signalling molecules. Recent work has shown that helper NLR resistosome clusters assemble upon activation of sensor NLRs, and that a wheat CCG10-NLR receptor forms an octameric resistosome. These structures represent a remarkable convergence with animal immunity, where inflammasomes perform analogous functions, and they explain how a single molecular recognition event can be amplified into a full-scale defensive response.

Perhaps the most important conceptual shift in recent years is the recognition that pattern-triggered immunity and effector-triggered immunity are not separate pathways but mutually reinforcing branches of a single system. Studies published in 2021 demonstrated that PRR signalling is required for full NLR-mediated resistance, and that activation of TIR signalling boosts pattern-triggered responses. The EDS1-PAD4-ADR1 node, a complex of lipase-like proteins and helper NLRs, mediates both branches, providing a molecular bridge between cell surface and intracellular perception. This mutual potentiation means that a plant that has already mounted a pattern-triggered response is primed to respond more vigorously to effector recognition, and vice versa. The review argues that this integration explains why plants with compromised PRR function are often more susceptible to disease even when they possess functional NLR genes.

But immunity is expensive. Uncontrolled activation of PRRs or NLRs causes stunted growth, autoimmunity and reduced seed yield, a phenomenon known as the growth-defence trade-off. Plants have evolved multiple mechanisms to keep immune signalling in check. Negative regulators such as the protein phosphatase PP2C38 dephosphorylate BIK1, while ubiquitin ligases control BIK1 protein homeostasis. The BAK1 co-receptor is shared between immune receptors and the brassinosteroid growth receptor BRI1, creating a molecular competition between defence and growth signalling. BIK1 inversely modulates these two pathways, promoting immunity while suppressing brassinosteroid responses. Membrane nanodomains physically separate immune and growth receptor complexes, even when they share signalling components. The review also describes how phytosulfokine signalling, mediated by the receptor PSKR1, balances growth and defence in the rhizosphere, and how transcription factors such as BZR1 mediate trade-offs at the gene expression level.

Environmental conditions add another layer of complexity. Temperature, light and humidity all modulate immune responses. Elevated temperatures can suppress NLR-mediated resistance, but recent work has identified CBP60g family transcription factors as key determinants of temperature sensitivity, offering a route to climate-resilient immunity. Light quality matters too: the blue-light receptor CRY1 acts as a switch that balances photosynthesis and defence, while phytochromes regulate salicylic acid and jasmonic acid pathways in rice. High humidity dampens salicylic acid signalling and NPR1 function, promoting disease, and daily humidity oscillations entrain the circadian clock to influence plant physiology. The microbiome also plays a role, with rhizosphere bacteria suppressing local root immune responses through pH modulation, and leaf microbiota influencing autoimmunity in Arabidopsis. The review presents a schematic model of these interplays, emphasizing that immunity cannot be understood in isolation from the environment.

The practical implications are profound. Understanding the mechanisms of immune receptor activation and regulation opens the door to engineering disease-resistant crops with optimized fitness. Researchers have transferred PRRs between plant families to confer broad-spectrum bacterial resistance, stacked multiple PRRs in potato against Phytophthora infestans, and used reverse engineering of FLS2 to expand recognition of evasive flagellin epitopes. NLR engineering has progressed from single amino acid mutations that expand effector recognition to designer receptors with novel specificities, nanobody fusions that redirect NLRs to new targets, and interfamily co-transfer of sensor and helper NLR pairs. Genome editing of susceptibility genes has produced multipathogen resistance without agronomic penalty, and inducible overexpression of transcription factors such as Ideal Plant Architecture1 improves both yield and disease resistance in rice. Machine learning and AlphaFold-guided design are now being applied to predict effector targets and redesign immune proteins. The review concludes that the next frontier lies in combining these engineering strategies with a deep understanding of growth-defence balance, so that crops can be made both resistant and productive in a changing climate.

Subject of Research: Mechanisms of pathogen perception, immune signalling and growth-defence balance in plant immunity

Article Title: Mechanisms and balanced regulation of plant immunity

Article References: Chai, J., Wang, Y., & Wang, Y. (2026). Mechanisms and balanced regulation of plant immunity. Nature Reviews Molecular Cell Biology. https://doi.org/10.1038/s41580-026-01009-4

Image Credits: AI Generated

DOI: 10.1038/s41580-026-01009-4

Keywords: plant immunity, pattern recognition receptors, NLR receptors, resistosomes, calcium signalling, growth-defence trade-off, effector recognition, immune receptor engineering, BIK1, BAK1, PTI, ETI

Salicylic acid has been recognized for centuries for its medicinal properties in humans, harkening back to willow bark remedies and culminating in the widely used drug aspirin. Parallel to its role in human health, SA operates as a master immune regulator in plants, orchestrating complex defense responses against a broad spectrum of microbial invaders and pests. Plants rely on finely tuned SA signalling pathways to activate defenses precisely where and when needed, balancing immune activation with the imperative to sustain healthy growth. The ability to map this delicate trade-off in living tissues has long been a formidable challenge for plant scientists.

The research team, led by Dr. Alexander Jones at the Sainsbury Laboratory Cambridge University, has now surmounted this obstacle by creating SalicS1, a biosensor that detects changes in SA within plants with exceptional sensitivity and specificity. By fusing SA-responsive elements to fluorescent proteins, the sensor emits signals that reflect real-time fluctuations of SA concentration. This tool empowers researchers to visualize how SA accumulation begins locally at infection sites and then spreads outwards into adjacent cells and tissues, providing direct evidence of the hormone’s dynamic propagation during immune responses.

Previous methods to study SA involved destructive sampling and biochemical assays that could only provide static, averaged data, masking the spatial-temporal complexity of SA signalling. With SalicS1, scientists can monitor live plants undergoing pathogen invasion, witnessing bursts of SA that travel cell-to-cell. This insight is crucial for unraveling how plants integrate localized defense cues to coordinate systemic immunity—or systemic acquired resistance—effectively priming distant tissues for potential threats. Understanding these processes is vital for engineering crops that can resist diseases while minimizing growth penalties associated with chronic immune activation.

Dr. Jones explains that pathogens such as fungi, bacteria, viruses, and even insect pests have evolved sophisticated mechanisms to suppress SA signalling, thereby dampening plant immunity and facilitating infection. By applying SalicS1, researchers can now dissect these pathogen strategies in real time and determine how plants counteract immune suppression. This knowledge is expected to inform innovative approaches to crop protection, enabling breeders and biotechnologists to enhance disease resilience in agriculture sustainably.

The work also highlights the reversibility and non-invasive nature of the biosensor measurements, which is a major technical advancement. Unlike traditional techniques that disrupt tissues, SalicS1 allows continuous monitoring of living tissues without collateral damage. This capability will enable detailed studies on how environmental stresses—such as drought or temperature extremes—intersect with immune signalling pathways, offering a holistic view of how plants manage competing physiological demands.

Importantly, the implications of SalicS1 transcend plant biology. Given that salicylic acid is the core precursor molecule to aspirin, the most widely used pharmaceutical worldwide, a modified version of the biosensor that detects aspirin could be adapted to investigate aspirin metabolism and cellular pharmacodynamics in human cells. Such a crossover application has the potential to open new frontiers in medical research, bridging plant science and human health.

First author Dr. Bijun Tang emphasizes the dynamic and localized nature of SA signalling unveiled by SalicS1. The ability to capture hormone surges at sites of pathogen ingress reveals the precise timing and intensity of immune activation, details previously inferred but not directly observed. This represents a leap towards understanding the biochemical warfare between plants and their myriad antagonists at a cellular level, dramatically refining the conceptual model of plant-pathogen interactions.

The team’s discovery also mirrors broader biological questions relevant to animal health, such as variability in individual responses to infections. Dr. Jones draws parallels to the COVID-19 pandemic, where pathogen exposure led to dramatically different outcomes among humans. Similarly, plants exposed to identical inoculation conditions exhibit variable immune successes, partly explained now through differential SA signalling patterns observable with SalicS1.

Ultimately, these insights pave the way for novel agricultural strategies that harness precise immune modulation rather than broad-spectrum chemical treatments. By breeding or engineering crops that can dynamically deploy SA responses when and where necessary, it may become feasible to reduce pesticide usage, promote sustainable farming practices, and ensure food security in the face of mounting pathogen pressures exacerbated by climate change.

The research, published in Science, was a collaborative effort involving several institutions, with critical technical contributions from the Institute of Experimental Botany of the Czech Academy of Sciences. Funding support was provided by the Gatsby Charitable Foundation, the European Research Council, the Max Planck Society, and EMBO. As this innovative biosensor is adopted and refined, it promises to illuminate the hidden molecular choreography that underpins plant survival and resilience, inspiring a new era in both plant science and beyond.

Subject of Research: Cells

Article Title: SALICYLIC ACID SENSOR1 reveals the propagation of an SA hormone surge during plant pathogen advance

News Publication Date: 9-Oct-2025

Web References:
Science Journal
DOI: 10.1126/science.adw7650

References:
Tang, B., Lu, J., Leontovyčová, H., Hoffmann, G., Rowe, J.H., O’Donnell, S.F., Grangé-Guermente, M., Larsen, B., Wimalasekera, R., Carella, P., Incarbone, M., Kalachova, T., Jones, A.M. (2025). SALICYLIC ACID SENSOR1 reveals the propagation of an SA hormone surge during plant pathogen advance. Science. DOI: 10.1126/science.adw7650

Image Credits: Bijun Tang

Keywords: Salicylic acid, plant immunity, biosensor, SalicS1, pathogen defense, hormone signalling, systemic acquired resistance, plant-pathogen interactions, fluorescence sensor, crop resilience, aspirin metabolism, cellular dynamics