Systems-level understanding of plant immune networks through single-cell and spatial omics.

Shared metabolic pathways in epilepsy and plant immunity: From evolution to diet.

NLR receptor subcellular localization and plant immune activation.

Salicylic acid (SA) and jasmonic acid (JA) play critical roles in regulating plant disease resistance. However, the underlying molecular mechanisms of their coordinated action against pathogens in woody plants, particularly in peach (Prunus persica), are unknown. In this study, we demonstrate that SA and JA positively regulate resistance to bacterial spot disease induced by Xanthomonas arboricola pv. pruni (Xap) in peach. Two defence-responsive genes, pathogenesis-related protein 2 (PpPR2) and PpPR5, were induced to express during this disease response. A key transcription factor, TGACG-BINDING FACTOR 1 (PpTGA1), functioned as a positive regulator of disease resistance by activating PpPR2 and PpPR5 transcription. Furthermore, nonexpressor of pathogenesis-related gene 1 (PpNPR1), a core component of the SA signalling response pathway, interacted with PpTGA1 to enhance transcriptional activation of PpTGA1 on downstream PR genes, thereby strengthening disease resistance. The JA signalling repressor, JASMONATE ZIM-DOMAIN 1 (PpJAZ1), negatively regulated disease resistance by interacting with PpTGA1 and inhibiting its transcriptional activation on the PRs. In summary, this study reveals an important regulatory network mediated by SA-JA hormone crosstalk for peach resistance to bacterial spot disease, based on the PpNPR1/PpJAZ1-PpTGA1-PpPR2/5 cascade. These findings provide novel insight into the synergistic crosstalk between hormones and the defence mechanisms against bacterial spot disease.

Mechanisms of Trichoderma-induced plant immunity: An RNA-epigenetic perspective.

Starvation as a weapon in fungal-plant warfare.

Valsa canker (caused by Cytospora mali = Valsa mali. C. mali) is one of the most destructive diseases affecting apple cultivation. The scarcity of natural germplasm resources with high resistance and immunity underscores the importance of exploring plant immune regulation factors of disease-resistant breeding. Protein post-translational modifications, particularly phosphorylation, are critical regulatory mechanisms in plant immunity. This study investigates how the apple receptor-like kinase MdRLKT1 modulates resistance to Valsa canker through the phosphorylation of the transcription factor MdRAX2. We found that MdRLKT1-interference (RNAi) transgenic lines exhibit increased susceptibility to C. mali infection compared to wild-type controls, indicating that MdRLKT1 positively regulates apple immune responses. Notably, MdRLKT1 interacts with the MYB transcription factor MdRAX2, facilitating its translocation into the nucleus. Invitro phosphorylation assays identified serine 147 (Ser147) as the phosphorylation site of MdRAX2 by MdRLKT1. Mutant MdRAX2S147A, with this phosphorylation site inactivated, demonstrated reduced resistance to C. mali. Further analysis revealed that MdRAX2 binds to the promoter region of MdMKS1, transcriptionally repressingits expression, whereas MdRAX2S147A failed to regulate MdMKS1 transcriptionally. Overexpression of MdMKS1 in apple resulted in reduced resistance to C. mali, suggesting that MdMKS1 negatively regulates apple immunity. These findings establish that the MdRLKT1-MdRAX2-MdMKS1 module plays a positive regulatory role in enhancing apple resistance to C. mali. In conclusion, MdRLKT1 activates the transcriptional repressor function of MdRAX2 through phosphorylation, thereby alleviating the negative regulatory effect of MdMKS1 on disease resistance and ultimately boosting the defensive capabilities of apple against pathogens.

Temporal dynamic and GhGLR4.8-mediated reorganization of 3D chromatin architecture during Fusarium oxysporum f. sp. vasinfectum infection in cotton.

Abstract Plant resistance genes play a critical role in enhancing crop immunity against various biotic stresses, such as pathogens, nematodes, and insects, safeguarding global agricultural productivity. A collection of plant resistance genes identified between 1992 and 2017 has been reported previously. To provide an updated overview of advances in research on plant resistance genes, we sorted out the mapped, identified, and cloned plant resistance genes reported from 2018 to the present. Data analyses revealed a total of 101 plant resistance genes reported since 2018, mainly from economically important crops (rice and wheat) and the model plant Arabidopsis thaliana , with a main focus on fungi, bacteria, and viruses. We subsequently conducted a bibliometric analysis of 9533 publications on plant resistance genes from the Web of Science core collection between 2007 and 2024. The number of publications increased from 334 in 2007 to 937 in 2024, significantly contributed by the institutions of the United States and China. Both the United States Department of Agriculture and the Chinese Academy of Agricultural Sciences are the top two institutions contributing to these publications. The top three journals in terms of publication volume are The Plant Cell, Journal of Integrative Plant Biology, and Plant Science. In addition, the leading journals Nature and Science published approximately 5% and 9% of these publications, respectively. Keywords analysis identified four primary research clusters: molecular mechanisms of plant resistance genes, plant immunity, wheat-specific resistance, and rice disease management. This study provides valuable insights into research trends, collaboration, and high-impact areas, serving as a resource for advancing plant resistance strategies to ensure global food security.

Summary Acclimation enables plants to adjust to immediate environmental fluctuations and is therefore key to the resilience of plant disease resistance in a time of climate change. Here, we report on the acclimation of Arabidopsis thaliana quantitative immune responses against the fungal pathogen Sclerotinia sclerotiorum to daily environmental fluctuations. We analyzed disease resistance phenotypes and global gene expression in plants grown in three acclimation regimes, revealing the rewiring of regulatory networks during this process. We identified pathogen‐induced genes weakly sensitive to acclimation as promising bases for acclimation‐proof immunity. Fluctuations in Mediterranean‐like acclimation resulted in an increased disease susceptibility and the misregulation of many pathogen‐responsive genes. We identified A. thaliana mutants in novel immune components contributing positively to quantitative disease resistance following temperate but not Mediterranean acclimation. Quantitative disease resistance was maintained under Mediterranean acclimation in NAC42‐like mutants and associated with a switch in the repertoire of pathogen‐responsive targets of this transcription factor. Our work reveals the role of immune gene networks' plasticity in acclimation and suggests new strategies to maintain plant immune function in a warming climate.

Ribosome-associated quality control (RaQC) pathways, including no-go decay (NGD) and non-stop decay (NSD), are essential for maintaining translational fidelity and regulating gene expression in eukaryotes. Central to these pathways is the conserved ribosome rescue factor PELOTA, which resolves stalled ribosomes and promotes the clearance of aberrant mRNAs and nascent polypeptides. While NGD and NSD have been extensively characterized in yeast and animals, our understanding of these processes in plants remains limited. Nevertheless, emerging evidence indicates that PELOTA plays a pivotal role in plant biology, contributing to key developmental processes and regulating immune responses to bacterial and viral pathogens. In this review, we provide an overview of the core NGD and NSD machinery in eukaryotes and synthesize current knowledge of these pathways in plants, highlighting both conserved mechanisms and regulatory features that appear to be plant-specific. We further discuss the roles of PELOTA in plant development and biotic stress responses and draw on insights from other eukaryotic systems to identify major gaps and open questions. By consolidating existing findings and outlining future research directions, this review aims to underscore the importance of ribosome-associated quality control in plants and aims to stimulate further investigation into this still underexplored field.

Lesion mimic mutants (LMMs) are ideal for dissecting plant immunity mechanisms. Here, we characterized lm10373, a stable LMM isolated from an EMS-induced library of wheat cultivar AK58. lm10373 developed light-dependent lesion spots on leaves from the late tillering stage, accompanied by programmed cell death (PCD) and reactive oxygen species (ROS) accumulation. Phenotypically, lm10373 showed reduced photosynthetic capacity and yield-related traits, but enhanced powdery mildew resistance at the heading stage. Genetic analysis revealed the lesion trait was controlled by a single semi-dominant nuclear gene, mapped to a 35 Mb interval on chromosome 3B via bulked segregant analysis coupled with exome capture sequencing (BSE-seq). Integrating exome sequencing and transcriptome data, we identified TaWSD1-3B (encoding an O-acyltransferase of the WSD1 family) as the causal gene. A G-to-A mutation (p.Ala79Thr) in its conserved acyltransferase domain introduced a new phosphorylation site, disrupting triacylglycerol biosynthesis. Two independent mutants (lm129, p.Arg207His; lm295, 3'UTR mutation) validated TaWSD1-3B function. Haplotype analysis of 183 wheat accessions identified three TaWSD1-3B haplotypes: Hap1 was associated with higher 1000-grain weight and lower leaf tip necrosis (LTN) severity, making it a favorable allele for breeding. This study characterized a wheat LMM mutant and candidate gene TaWSD1-3B, suggesting a lipid-ROS-PCD pathway regulating immunity, and provides valuable markers for stress-tolerant, high-yield wheat breeding.

Ralstonia solanacearum poses a severe threat to global agriculture due to its broad host range, high dispersal capacity, and limited chemical control options. Plant immune inducers provide an effective strategy for controlling bacterial wilt disease. This study demonstrated a natural-derived compound esculetin (ES) serves as a novel plant immune inducer against tobacco bacterial wilt. Foliar application of ES exhibits considerable control effect on tobacco bacterial wilt, with control efficacy is high as 45.41%-68.69%, significantly higher than positive control treatment-benzothiadiazole (BTH). ES activates systemic acquired resistance (SAR) by upregulating transcriptional level of pathogenesis-related (PR) genes, inducing reactive oxygen species (ROS) burst, enhancing defense-related enzyme activity and salicylic acid (SA) accumulation. Transcriptomic analyses reveal that ES induces expression of mitogen-activated protein kinase (MAPK) signaling pathways, SA biosynthesis, phenylpropanoid pathway and brassinosteroid biosynthesis pathway. Furthermore, ES confers broad-spectrum resistance against other diseases like tobacco target spot, tobacco mosaic virus (TMV), wildfire disease and tobacco black shank. The study reveals a novel plant immunity inducer ES that confers broad-spectrum resistance against R. solanacearum by activating the SA-mediated SAR pathway, which provides a sustainable application of ES on bacterial wilt and other plant diseases in the future. © 2026 Society of Chemical Industry.

Abstract Nucleotide-binding leucine-rich repeat receptors (NLRs) are central to plant immunity, yet the mechanisms regulating their homeostasis remain poorly understood. In this study, we identify StRWA2 as a susceptibility factor in potato (Solanum tuberosum) that negatively regulates NLR-mediated resistance to Phytophthora infestans. StRWA2 destabilizes NLR proteins R3a and Rpi-blb2 via the 26S proteasome, suppressing NLR-mediated hypersensitive responses (HR). Mechanistically, StRWA2 recruits the E3 ubiquitin ligase StSNIPER2 (SNC1-INFLUENCING PLANT E3 LIGASE REVERSE 2) and enhances its E3 ligase activity, enabling StSNIPER2-dependent ubiquitination and degradation of NLRs. Furthermore, we confirm the necessity of this partnership, which silencing NbSNIPER2a/b reduced StRWA2-mediated plant susceptibility, while expression of a ligase-dead StSNIPER2 variant (StSNIPER2H123Y) restored NLR stability and plant resistance. Crucially, we obtained StRWA2-silenced potato plants via the RNA interference (RNAi), which conferred resistance to P. infestans with no observable growth penalties compared to wild-type controls. Together, this study identified a susceptibility factor RWA2 from potato that recruits the E3 ligase SNIPER2 to destabilize NLRs. Our findings reveal a critical NLR regulation mode and propose RWA2 as a promising target for engineering disease resistance in crops.

WD40 proteins are key regulators of defensive metabolism and stress adaptation, promising targets for engineering stress-tolerant woody species. Through genome-wide analysis, we identified 231 PfWD40 genes in Paulownia fortunei, establishing the first WD40 genomic resource in Paulowniaceae and revealing its domain architectures and expansion patterns. Expression profiling showed 32, 67, and 76 PfWD40 genes differentially expressed under salt, drought, and phytoplasma stress, respectively. PfWD40-98 and PfWD40-116 interact with the WRKY protein PfTG21 and modulate flavonoid biosynthesis. Importantly, we provide the first evidence that phytoplasma effectors (Pawb3, Pawb19, Pawb51) directly target these regulatory PfWD40 proteins, validated by Y2H and BiFC assays. Molecular docking identified key residues governing these interfaces. This study establishes the first WD40 genomic resource in Paulownia and reveals a previously unreported pathogenic strategy─effector-mediated hijacking of a host WD40 hub─offering molecular insights for developing stress-tolerant and disease-resistant woody plants.

Plant diseases caused by biotic and abiotic stresses pose a great threat to both plant health and yield. Plant microbiomes play a crucial role in improving disease resistance, representing a sustainable approach to enhance crop performance. Plant host factors, including genetic variation, metabolites and microRNA, shape the assembly and function of the plant microbiome, thereby augmenting disease resistance. This interplay presents opportunities for plant-mediated manipulation of microbiome to promote plant health. Multiple mechanisms are involved in the microbiome-mediated plant disease resistance, such as direct and indirect pathogen antagonism, niche pre-emption, alteration of microbiota and activation of plant defences. Nevertheless, the application of plant microbiome in the field remains limited due to the intrinsic complexity of plant-microbiome and environment-microbiome interactions. This review synthesises current knowledge on the roles of plant microbiomes in plant disease resistance. I further summarise the mechanisms underlying plant-guided microbiome modulation and probiotic-mediated disease suppression. I also raise work and challenges that should be addressed, with the ultimate goal of informing more efficient microbiome application in sustainable agriculture.

Receptor-like proteins (RLPs) are key components in the plant immune system. Loss of the RLP SUPPRESSOR OF NPR1-1, CONSTITUTIVE 2 (SNC2) in Arabidopsis results in enhanced disease susceptibility, whereas the gain-of-function mutant snc2-1D exhibits autoimmunity including a dwarfed morphology and constitutively activated defense responses. SNC2 function is fully dependent on the transmembrane protein BIAN DA 1 (BDA1). SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1 (SARD1) and CALMODULIN-BINDING PROTEIN 60 g (CBP60g) are two transcription factors required for the autoimmunity of snc2-1D. Constitutive defense responses in snc2-1D are attenuated by the cbp60g single mutant, but fully abolished by the sard1 cbp60g double mutant. In this study, we identified and characterized the ADAPTOR PROTEIN 4 (AP4) complex in SNC2-mediated plant immunity. By performing a suppressor screen in the cbp60g-1 snc2-1D background, mutations in AP4μ, a subunit of the AP4 complex, were identified. Interestingly, AP4μ associates with BDA1, and Y18 and Y257 of BDA1 seem to play important roles in such interaction. Knocking out genes of other subunits in the AP4 complex consistently suppressed cbp60g-1 snc2-1D autoimmunity, suggesting that the AP4 complex is required for SNC2 signaling. Furthermore, mutating AP4μ in wild-type plants compromises basal defense and pattern- and effector-triggered immunity, indicating a broader role of the AP4 complex in plant immunity.

Nicotinamide mononucleotide confers broad-spectrum disease resistance in plants

Viral action on the auxin signaling repressor IAA16 reveals a conserved negative regulator of plant growth and immunity.

Burkholderia seminalis suppresses Fusarium wilt infection in banana by modulating cell wall integrity.