How Plants Strike a Balance Between Immune Power and Growth

Plants cannot run from their enemies, so they have evolved an extraordinary arsenal of molecular sentinels that detect invading pathogens and launch defences within minutes. Yet this vigilance comes at a price: every burst of immune activity diverts energy, nutrients and hormones away from growth and reproduction. A new review published in Nature Reviews Molecular Cell Biology by Jijie Chai of Westlake University and Yuanchao Wang and Yan Wang of Nanjing Agricultural University synthesizes the latest structural and mechanistic insights into how plants perceive pathogens, how immune signals travel from receptor to response, and how the plant body keeps this powerful machinery in check so that defence does not come at the expense of fitness. The review arrives at a moment when the field is converging on a unified picture of plant immunity, one in which two previously separate branches of the immune system are now understood to work together rather than in isolation.

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