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Scooped by
The Sainsbury Lab
June 16, 10:12 AM
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Intracellular immune receptors protect plants from microbial invasion by detecting and responding to pathogen-derived effector molecules, often triggering cell death responses. However, pathogen effectors can evolve to avoid immune recognition, resulting in devastating diseases that threaten global agriculture. Here, we show that an integrated Exo70 domain from the barley intracellular nucleotide-binding leucine-rich repeat (NLR) RGH2 can interact with both the rice blast pathogen effector AVR-Pii and a closely related wheat blast causing variant. We used structure-led engineering to develop RGH2+ that shows increased binding affinity towards AVR-Pii variants and increased cell death responses on heterologous expression in Nicotiana benthamiana. Infection assays in transgenic barley lines carrying RGH2+ with the paired NLR RGH3 indicate a reduced susceptibility to blast strains expressing AVR-Pii variants. These results demonstrate the potential of engineering NLR receptors as an effective strategy for improving resistance towards one of the most destructive diseases affecting cereal production.
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Scooped by
The Sainsbury Lab
June 8, 11:06 AM
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Pathogens counteract central nodes of NLR immune receptor networks to suppress immunity. However, the mechanisms by which pathogens hijack helper NLR pathways are poorly understood. We show that an effector from the late blight pathogen Phytophthora infestans interacts with the host protein NbTOL9a and a helper NLR to suppress immunity. We solved the crystal structure of the RXLR-LWY effector AVRcap1b in complex with the ENTH domain of NbTOL9a. The structure revealed that, unlike other RXLR-LWY effectors, AVRcap1b has a previously unidentified L-shaped fold that defines a distinct structural family of effectors in the genus Phytophthora. We defined the AVRcap1b/NbTOL9a binding interface and designed effector mutants that do not bind NbTOL9a, impairing immune suppression. This suggests that ENTH binding is required for full virulence activity. Last, we show that AVRcap1b associates specifically with activated NbNRC2 independently of NbTOL9a binding. We propose a model in which the effector interconnects NbNRC2 with the NbTOL9a pathway. Our results illustrate a previously uncharacterized pathogen mechanism to hijack NLR pathways and suppress immunity.
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Scooped by
The Sainsbury Lab
June 8, 9:37 AM
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The blast fungus Magnaporthe oryzae infects plants using an appressorium that generates force to breach the leaf cuticle. Appressorium development follows a cell-cycle-regulated morphogenetic program requiring autophagy-associated death of the spore. How proliferative growth is coordinated with cell death remains unclear. Here, we show that each conidial cell follows a distinct developmental program essential for infection. Using quantitative live-cell imaging, we tracked 10 organelle types during appressorium morphogenesis in wild-type and Δatg8 mutant strains. Photoactivatable GFP microscopy revealed that mitochondria traffic from a single conidial cell into the appressorium, while the remaining cells undergo autophagy. Organelle inheritance occurs independently of cell-cycle checkpoints but coincides with spore germination. Photoconvertible fluorescence microscopy defined the temporal sequence of organelle movement and de novo biogenesis. Our findings reveal that coordinated spatiotemporal control of autophagy and organelle trafficking is necessary for rice blast infection.
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Scooped by
The Sainsbury Lab
June 8, 9:22 AM
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Diploid potato breeding enables faster genetic improvement via selection against deleterious alleles in inbred lines, unlike breeding by intercrossing tetraploid varieties. Starch is the major source of calories in potato tubers, but the starch properties of diploid lines have rarely been reported. In this study, we provide a comprehensive characterisation of tuber and starch properties in two diploid lines that are early isolates from the Solynta breeding program, B26 and B100, and their F1 hybrids. B100 produced fewer, but larger tubers compared to B26, and both diploid lines produced tubers that are smaller than the tetraploid variety, Clearwater Russet. The low tuber yield of B100 correlates with its high self-compatibility and fruit production. Pruning of fruits in B100 significantly increased total tuber yield per plant by stimulating more tuber initiations, but had no effect on average tuber weight, starch content or starch structure. Among the diploid, hybrid and tetraploid lines examined, there were no differences in the total starch content of tubers. Although amylopectin structure and amylose content were similar between the two diploid lines and the tetraploid comparison, B26 had elevated levels of resistant starch and a striking elongated granule morphology. Our results showcase the variation in source-sink relations and starch structure in diploid potato breeding material, demonstrating their potential for research into the genetics underpinning metabolic and quality traits.
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Scooped by
The Sainsbury Lab
May 27, 6:09 AM
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Non-host resistance refers to the immunity of plant species to virtually all isolates of a potential pathogen and represents an underexplored avenue for breeding and engineering disease resistance. In domesticated and wild barley, cell surface-localized lectin receptor kinases (LecRKs) contribute to determining the host status to leaf rust fungi, which pose a major threat to global cereal production. Here, we identify a conserved family of leaf rust glycoside hydrolases as ligands for these barley LecRKs and show that direct ligand-receptor binding triggers immune responses. This mechanism of pathogen perception is conserved across multiple cereal species and can be functionally transferred between them. We also uncover previously uncharacterized recognition specificities among distinct LecRK variants, expanding the repertoire of LecRK-mediated rust pathogen detection. Our findings define a molecular mechanism underlying non-host resistance in cereals and provide a basis for harnessing non-host rust resistance across diverse crop-pathogen systems.
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Scooped by
The Sainsbury Lab
May 22, 7:39 AM
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NLR immune receptor networks consist of expanded disease resistance proteins (sensor NLRs) that signal via core executors of immunity known as helper NLRs. Although some sensor NLRs are thought to activate their cognate helpers via an activation-and-release mechanism, the structural basis of sensor-helper communication remains poorly understood. Here, we identify and validate sensor-helper NLR interfaces that are critical for immune activation in the NRC network of coiled-coil NLR immune receptors. Using AlphaFold 3 we predicted a high confidence model between the virus resistance protein Rx and its helper NLR NRC2. We validated the interfaces by loss and gain-of-function mutagenesis, including reconstituting a critical salt bridge through reciprocal mutations. We showed that these interfaces are conserved across the NRC network of asterid plants despite over 120 million years of divergence and validated the sensor-NRC interfaces within the common lettuce network. Structure-guided bioengineering of a lettuce sensor NLR enabled expansion of its NRC helper compatibility profile. These results are consistent with the activation-and-release model and point to bioengineering sensor-helper specificity in economically important crop species.
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Scooped by
The Sainsbury Lab
May 21, 9:13 AM
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Artificial intelligence (AI) systems such as AlphaFold have transformed structural biology by enabling accurate prediction of protein structures. However, their capacity to uncover new classes of macromolecular assemblies remains largely untapped. We developed the Structural Novelty Index (SNI), a quantitative framework for identifying protein complexes that diverge from canonical architectures. As one implementation of SNI, we developed SNINRC-Hexa, to identify unconventional resistosomes formed by nucleotide-binding, leucine-rich repeat immune receptors (NLRs). We used it to analyze AlphaFold 3 models of 637 non-redundant NRC proteins from 346 genomes representing 85 plant species. This analysis identified candidates with predicted architectures distinct from the canonical hexameric resistosomes of NRC proteins. Biochemical purification and negative-stain transmission electron microscopy of NRC7 orthologs from multiple species supported the SNI prediction and revealed an unexpected undecameric (11-mer) assembly. Our results establish SNI as a scalable approach for discovering atypical protein complexes.
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Scooped by
The Sainsbury Lab
April 30, 9:57 AM
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Bacteria-derived lipopeptides are immunogenic triggers of host defences in metazoans and plants. Root-associated rhizobacteria produce cyclic lipopeptides that activate induced systemic resistance against microbial infection in various plant species. Whether and how these molecules are perceived at the plant cell surface remains elusive. Here we reveal that immune activation in Arabidopsis thaliana by the lipopeptide elicitor surfactin is mediated via a specific interaction with membrane sphingolipids. It relies on host membrane remodelling and subsequent activation of mechanosensitive ion channels. This mechanism leads to host defence potentiation and resistance to the necrotrophic fungus Botrytis cinerea and appears distinct from pattern-triggered immunity induced by classical host pattern recognition receptors. These results reveal a previously uncharacterized mechanism through which lipopeptides derived from non-pathogenic bacteria activate plant immune responses. This work unveils a non-canonical lipid-driven mechanism for plant immune activation by a bacterial lipopeptide. Perception at the cell membrane leads to deformation, mechanosensing and early signalling and culminates in systemic resistance priming.
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Scooped by
The Sainsbury Lab
April 27, 4:18 AM
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Dioecious plants, which have distinct male and female individuals, constitute ~5% of angiosperm species and have emerged frequently and independently from hermaphroditic ancestors. Although recent molecular studies of sex determination have started to reveal the diversity of the genetic systems underlying dioecy, research on the evolution of dioecy is limited, especially in monocots. Here, we explore the molecular basis of sex determination in the monocot Dioscorea tokoro, a dioecious wild yam endemic to East Asia. Chromosome-scale and haplotype-resolved genome assemblies and linkage analysis suggested that this plant has a male heterogametic sex-determination (XY) system, with sex-determination regions located on chromosome 3. Sequence comparison between the X- and Y-chromosomes and read coverage analysis revealed X- and Y-specific regions in putative pericentromeric chromosome regions. Within the Y-specific region, we propose two candidate genes that are likely involved in sex determination: BLH9, encoding a homeobox protein, and HSP90, encoding a molecular chaperone. BLH9 functions in a similar way as AtBLH9 in Arabidopsis thaliana. BLH9 could be involved in suppression of female organ development, whereas HSP90 might be required for pollen development. These results shed light on the complex evolution of dioecy in plants.
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Scooped by
The Sainsbury Lab
April 23, 4:22 AM
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Extracellular alkalinization has long been recognized as a hallmark of plant cell-surface receptor activation, including during pattern-triggered immunity (PTI), yet the mechanisms driving elicitor-induced alkalinization and its role in plant signaling remain unclear. Here, we demonstrate that inhibition of autoinhibited H+-ATPases (AHAs) is required for elicitor-induced extracellular alkalinization. This alkalinization is essential for immune and cell-wall damage signaling mediated by diverse plasma membrane-localized receptor kinases (RKs), likely through modulation of ligand-receptor interactions. Mechanistically, RKs transduce elicitor-triggered signaling via the receptor-like cytoplasmic kinase BOTRYTIS-INDUCED KINASE 1 (BIK1), which inhibits AHA activity by disrupting AHA-GENERAL REGULATORY FACTOR (GRF) interactions through a conserved phosphorylation event. This phosphorylation-driven extracellular alkalinization module is required for disease resistance and cell-wall damage responses initiated by ligand-RK pairs. Our findings uncover a conserved phosphorelay circuit that broadly regulates extracellular alkalinization to coordinate RK signaling, illuminating a general mechanism for RK activation and stress resilience.
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Scooped by
The Sainsbury Lab
April 8, 4:31 AM
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Plants secrete a variety of proteases as a defense response during infection by microbial pathogens. However, the relationship between their catalytic activities and antimicrobial functions remains largely unknown. Particularly, few biologically relevant substrates of these proteases have been identified. Huanglongbing (HLB) has been a major threat to the citrus industry worldwide. The HLB-associated bacterium, "Candidatus Liberibacter asiaticus" (Las), was previously shown to deploy an inhibitor of papain-like cysteine proteases (PLCPs) to promote disease in citrus. In this study, we identified an outer membrane protein (OMP) of Las, LasOMP1, as a substrate of the citrus PLCP CsRD21a. LasOMP1 is one of the most highly expressed genes in Las. CsRD21a cleaves LasOMP1 and produces cleaved peptide products, which could be detected in vitro and in HLB-diseased citrus plants. We found that CsRD21a targets the N-terminal portion of LasOMP1, potentially at an extracellular loop region. Importantly, transgenic sweet orange overexpressing CsRD21a showed reduced Las populations and improved plant growth, highlighting that engineering this protease is a promising strategy to enhance HLB resistance in citrus. Together, our work reveals a pathogen-derived substrate of plant PLCPs and suggests bacterial OMPs may be direct targets of plant defense.
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Scooped by
The Sainsbury Lab
March 31, 11:16 AM
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The wheat blast fungus Magnaporthe oryzae pathotype Triticum (MoT) poses a severe threat to global wheat (Triticum aestivum L.) production, yet the molecular mechanisms underlying tissue invasion remain poorly understood. We performed dual RNA-seq analysis of MoT-inoculated wheat leaves at 0, 24, 36, and 48 hpi, mapping reads separately to the wheat and M. oryzae genomes to capture stage-specific host responses and pathogen gene expression across progressive infection stages. Wheat exhibited pronounced stage-specific transcriptional reprogramming, with peak differential gene expression at 36 hpi and visible symptoms at 48 hpi. The 24 hpi stage was characterized by rapid induction of immune- and defense-related pathways, including innate immunity and detoxification processes, along with downregulation of cell wall and membrane biosynthesis. By 36 hpi, wheat maintained sustained activation of immune and detoxification pathways, while chloroplast- and photosynthesis-associated genes were broadly repressed, consistent with transcriptional features of metabolic constraint. At 48 hpi, coinciding with lesion initiation, transcriptomes showed persistent, metabolically costly immune and defense responses together with extensive suppression of photosynthesis- and chloroplast-associated functions, which were associated with metabolic strain and a transition toward necrosis. Analysis of pathogen-derived reads revealed temporal induction of multiple effector candidates, including known M. oryzae orthologs and additional effector-like proteins, highlighting coordinated temporal patterns between host immune and metabolic response as well as stage-specific pathogen effector expression. Together, these findings provide a temporal framework for wheat blast susceptibility and highlight key host pathways and effector candidates that define critical windows for functional dissection of MoT virulence and wheat susceptibility.
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Scooped by
The Sainsbury Lab
March 31, 11:10 AM
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Photoperiodism, a seasonal response mechanism that relies on day-length measurement by the circadian clock, is a major regulator of flowering time (Imaizumi 2025). The external coincidence model proposes that the alignment between the internal circadian phase and external light signals triggers photoperiodic responses (Pittendrigh and Minis 1964). It has been challenging to establish robust models for the quantitative relationship between clock and flowering time, due to a lack of tools to modulate the clock quantitatively. Here, using a circadian period-lengthening small molecule, we demonstrated the quantitative modulation of the critical day-length for flowering in monocots.
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Scooped by
The Sainsbury Lab
June 8, 11:10 AM
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Helper NLRs function as central nodes in plant immune networks. Upon activation, they oligomerize into inflammasome-like resistosomes to initiate immune signaling, yet the dynamics of resistosome assembly remain poorly understood. Here, we show that the virulence effector AVRcap1b from the Irish potato famine pathogen Phytophthora infestans suppresses immune activation by directly engaging oligomerization intermediates of the tomato helper NLR SlNRC3. Cryo-EM structures of SlNRC3 in AVRcap1b-bound and unbound states reveal that AVRcap1b bridges multiple protomers, stabilizing a stalled intermediate and preventing formation of a functional resistosome. Leveraging AVRcap1b as a molecular tool, we also capture an additional SlNRC3 resistosome intermediate showing that assembly proceeds in a stepwise manner from dissociated monomers. These findings uncover a previously unrecognized vulnerability in NLR activation and reveal a pathogen strategy that disrupts immune complex assembly. This work advances mechanistic understanding of resistosome formation and uncovers a previously unrecognized facet of pathogen-plant coevolution.
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Scooped by
The Sainsbury Lab
June 8, 9:43 AM
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Plants and animals respond to pathogen attack by mounting innate immune responses that require intracellular nucleotide-binding leucine-rich repeat (NLR) proteins. These immune receptors detect pathogen infection by sensing virulence effector proteins. However, how receptors evolve new recognition specificities remains poorly understood. We found that the plant NLR MLA3 (Mildew locus a 3) has evolved to recognize a pathogen effector by acting as a molecular mimic of an effector virulence target, thereby triggering an immune response. By introducing the mimic’s binding interface into the wheat stem rust resistance protein SR50, we bioengineered a chimeric receptor with dual recognition activities that conferred resistance to two major cereal pathogens in barley transgenic lines. These results demonstrate that molecular mimicry by immune receptors can be harnessed to engineer multiple disease resistance.
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Scooped by
The Sainsbury Lab
June 8, 9:33 AM
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Host-induced gene silencing (HIGS) is a crop protection strategy that exploits RNA interference (RNAi) to silence targeted genes in invading pathogens or pests and reduce disease. Despite some successful examples of HIGS in laboratory settings, its translation into commercial agriculture has been limited. Recent discoveries demonstrating that plants deploy specific endogenous small RNAs (sRNAs) to regulate gene expression in fungi and oomycetes have broadened our understanding of natural trans-species RNAi (natural-tsRNAi) and provided a framework for improving applications of sRNA-based defense. In this review, we summarize HIGS studies published between 2021 and 2025 with a meta-analysis, highlighting their potential and limitations. We then discuss recent advances in natural tsRNAi with an emphasis on the secondary small interfering RNA pathway as a native immune response. Finally, we provide our opinion on how insights from natural tsRNAi inform design principles for sRNA-based immunity as a promising source of engineering durable resistance traits.
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Scooped by
The Sainsbury Lab
May 29, 2:26 AM
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The blast fungus Magnaporthe oryzae is the causal agent of the most serious disease of cultivated rice and an emerging threat to wheat production. Controlling blast diseases is therefore critical to ensuring global food security. In this review, we describe the mechanism by which the fungus ruptures the plant cuticle to gain entry to host cells and the virulence determinants necessary for suppression of host immunity and rapid colonization of plant tissue.
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Scooped by
The Sainsbury Lab
May 22, 10:36 AM
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Toll/interleukin-1 receptor (TIR) enzymes are prominent immune components in diverse organisms across the tree of life. In flowering plants, TIRs are often integrated into nucleotide binding leucine-rich repeat (NLR) receptors whose oligomerization-dependent biochemical activities create second messengers perceived by ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1)-family signaling complexes. TIR-NLRs and TIR proteins are present across the full spectrum of plant evolution, yet EDS1 signaling is a derived trait in seed plants. Here, we examined the functional dependency of diverse plant TIRs on the EDS1 pathway in the angiosperms Nicotiana benthamiana and Nicotiana tabacum. While the isolated TIR domains from non-seed plants generally required EDS1 for immune cell death activation, we also identified TIRs that functioned independent of EDS1. However, chimeric TIR-NLRs incorporating these diverse TIR domains onto the AtWRR4a receptor chassis showed a full reversion to EDS1-dependency. Extending this phenomenon further, we demonstrated that the AtWRR4a architecture enforces EDS1-dependence onto a bacterial TIR domain that is otherwise EDS1-independent. Collectively, our work demonstrates that NLR immune receptor architecture influences TIR-related immunity and provides further context to their ancient acquisition into plant immune systems.
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Scooped by
The Sainsbury Lab
May 22, 6:26 AM
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To establish infection, phytopathogens deploy effectors to compromise host defences and facilitate invasive growth. As part of this, the battle for control of symplastic connectivity via plasmodesmata is a key determinant of infection outcomes, yet little is known about how fungal effectors directly exploit these channels, and in turn, how hosts defend them. Here, we have identified ChEC108 as a plasmodesmal-targeting, cell-to-cell mobile effector from the anthracnose fungus, Colletotrichum higginsianum. ChEC108 binds the plasmodesmal protein HEAVY METAL-ASSOCIATED (HMA) ISOPRENYLATED PLANT PROTEIN 6 (HIPP6) from Arabidopsis via a tetrahedral metal ion coordination site with either of its HMA domains. Constitutive in planta expression of ChEC108 induces plasmodesmal closure and the upregulation of defence-associated genes in a manner dependent on its capacity to bind HIPP6. Further, HIPP6 binding impairs cell-to-cell mobility of ChEC108. Alongside the finding that loss of ChEC108 favoured C. higginsianum infection, this suggests ChEC108-HIPP6 interaction at plasmodesmata positively regulates defence.
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Scooped by
The Sainsbury Lab
May 1, 10:10 AM
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Upon activation, plant nucleotide-binding leucine-rich repeat (NLR) immune receptors are known to assemble into oligomeric resistosomes that insert into the plasma membrane, forming calcium (Ca2+)–permeable channels and triggering immunity. Here, we found that the RPW8-like coiled-coil NLR (CCR-NLR) N requirement gene 1 (NRG1) primarily targets organelles instead of the plasma membrane. Unlike canonical CC-NLRs, activated NRG1 accumulated at the chloroplast envelope and channeled stromal Ca2+ into the cytosol. AlphaFold modeling of the NRG1 resistosome revealed an unusually long amino-terminal membrane-insertion structure that could span the double membrane of the chloroplast. Nanobody-mediated relocalization showed functional membrane specificity: Chloroplast trapping abolished activity of the canonical helper CC-NLR NRC4 but not NRG1. NRG1 orthologs, from nonflowering lineages to angiosperms, targeted chloroplasts, suggesting that organelle-centered defense dates back at least ~360 million years. We propose that CC-NLR diversification has enabled compartment-specific immune signaling to capture diverse Ca2+ stores.
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Scooped by
The Sainsbury Lab
April 28, 7:52 AM
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Plant diseases remain a major threat to food security, reducing crop yield worldwide. A central challenge in crop protection is that effective immunity often comes at a cost. Plants must continuously balance growth with defense, and this balance complicates molecular breeding strategies aimed at improving disease resistance. When immune pathways are constitutively activated, plants are often better protected against pathogens, but the price for this protection is reduced growth or fitness. This defense-growth trade-off has therefore become a major obstacle to engineering disease resistance in crops.
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Scooped by
The Sainsbury Lab
April 23, 8:54 AM
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When organisms encounter pathogens, they rapidly activate complex defense programs to ensure survival. While these immune responses are vital, they often also incur trade-offs, such as reduced growth and development and must therefore be tightly controlled. In this study, we reveal that the steroid hormones brassinosteroids (BRs) contribute to this control in Arabidopsis thaliana by repressing immunity-related genes. We provide evidence that the BR-regulated basic helix-loop-helix (bHLH) transcription factor CESTA (CES), along with its homologs BR ENHANCED EXPRESSION (BEE)1-3, mediate DNA methylation changes at transposable element (TE)-rich loci containing nucleotide-binding leucine-rich-repeat (NLR)-type receptor genes, including SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1 (SNC1). These CES-induced methylation changes correlate with altered splicing of SNC1 pre-mRNA, a process that requires the BR receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1). In support, we show that CES associates with components of the chromatin remodeling and splicing machinery. Together, our findings reveal a previously unrecognized BR-induced mechanism that modulates the epigenetic and post transcriptional regulation of immune genes, enabling plants to prioritize growth over defense.
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Scooped by
The Sainsbury Lab
April 22, 6:27 AM
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Extracellular vesicles (EVs) transport biologically active molecules and are known to mediate host defence against microbial pathogens, including plant fungal pathogens. However, the mechanism by which pathogens disrupt EV-dependent defence remains unclear. Here we show that Phytophthora capsici, a global crop pathogen, counteracts EV-mediated plant defence through targeted lipase activity. We show that Arabidopsis releases EVs containing tetraspanin (TET), specifically TET8- and TET9-EVs, which damage germinated spores of Phytophthora, reducing infection. As a counter-defence, Phytophthora secretes an infection-induced apoplastic lipase, Plant Extracellular Vesicle Destroyer 1 (PED1), which targets TET8- and TET9-EVs. This occurs via interaction with the EV membrane-localized protein Defective Glycosylation 1 (DGL1), which directly interacts and co-localizes with TET8 and TET9 on the EV membrane. PED1 damages TET8- and TET9-EVs through its lipase activity towards campesteryl esters, suppressing EV-mediated plant defence. Our study reveals a mechanism used by Phytophthora to counteract EV-mediated host defence. Phytophthora secretes an infection-induced apoplastic lipase, damaging Arabidopsis extracellular vesicles and suppressing plant defence against infection.
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Scooped by
The Sainsbury Lab
April 7, 6:09 AM
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Septin GTPases are essential cytoskeletal regulators that organize membranes and scaffold protein complexes to control cytokinesis, polarity, and morphogenesis. How septins execute these functions remains poorly understood, and comprehensive, stage-resolved interaction maps are lacking. Here, we define a quantitative, time-resolved septin interactome in the rice blast fungus Magnaporthe oryzae using immunoprecipitation coupled to mass spectrometry. We map more than 350 interactors of septins Sep3, Sep4, Sep5 and Sep6, revealing a dynamic network required for appressorium-mediated plant infection. Beyond canonical roles in cytoskeletal organisation and polarity, septins associate with proteins linked to membrane remodelling, metabolism, and virulence, deployed during host invasion. Integration with ultra-high-throughput yeast two-hybrid analysis defines a high-confidence septin interactome and identifies previously uncharacterised factors, including Msi1, a BAR domain protein required for invasive growth. Together, these findings establish septins as dynamic organisers of infection-related processes and provide a framework for understanding how cytoskeletal scaffolds coordinate fungal pathogenesis.
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Scooped by
The Sainsbury Lab
March 31, 11:12 AM
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Nucleotide-binding, leucine-rich repeat (NLR) receptors are widespread intracellular immune sensors across kingdoms. Plant G10-type coiled-coil (CCG10)-NLRs constitute a distinct phylogenetic clade that remains poorly characterized. Here, we identified a gain-of-function mutant of wheat autoimmunity 3 (WAI3GOF), which encodes a constitutively active CCG10-NLR resulting from a residue substitution in the leucine-rich repeat (LRR) domain. Cryo-electron microscopy (cryo-EM) analysis reveals that activated WAI3 assembles into a distinctive octameric resistosome. Arabidopsis RPS2, another CCG10-NLR, also forms an octamer, indicating a conserved structural property across monocot and dicot plants. The WAI3 resistosome induces a prolonged and sustained increase in cytosolic calcium, likely facilitated by a unique channel architecture arising from its divergent coiled-coil (CC) domain configuration. Notably, this domain arrangement may be shared by plant NLRs that lack the conserved EDVID (Glu-Asp-Val-Ile-Asp) motif in their CC domains. Together, our findings uncover a conserved yet previously uncharacterized NLR resistosome structure and provide insights into the plant immune receptor plasticity.
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