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The plant epidermis is the first line of plant defense against pathogen invasion, and likely contains important regulatory proteins related to the plant–pathogen interaction. This study aims to identify the candidates of these regulatory proteins expressed in the plant epidermis. We performed comparative proteomic studies to identify rapidly and locally expressed proteins in the leaf epidermis inoculated with fungal phytopathogen. The conidia solutions were dropped onto the Arabidopsis leaf surface, and then, we collected the epidermal tissues from inoculated and mock-treated leaves at 4 and 24 hpi. The label-free quantification methods showed that expressions of Arabidopsis proteins, which are related to defense signals, such as BAK1, MKK5, receptor-like protein kinases, transcription factors, and stomatal functions, were rapidly induced in the epidermal tissues of inoculated leaves. In contrast, most of them were not differentially regulated by fugal inoculation in the whole leaves. These findings clearly indicate that epidermal proteomics can monitor locally expressed proteins in inoculated areas of plant tissues. We also identified the 61 fungal proteins, including effector-like proteins specifically expressed on the Arabidopsis epidermis. Our new findings suggested that epidermal proteomics is useful for understanding the local expressions of plant and fungal proteins related to their interactions.

Summary In photosynthetic cells, plants convert carbon dioxide to sugars that can be moved between cellular compartments by transporters before being subsequently metabolized to support plant growth and development. Most pathogens cannot synthesize sugars directly but have evolved mechanisms to obtain plant‐derived sugars as C resource for successful infection and colonization. The availability of sugars to pathogens can determine resistance or susceptibility. Here, we summarize current progress on the roles of sugar transporters in plant–pathogen interactions. We highlight how transporters are manipulated antagonistically by both host and pathogens in competing for sugars. We examine the potential application of this target in resistance breeding and discuss opportunities and challenges for the future.

Rice ( ) is the leading source of nutrition for more than half of the world's population, and by far it is the most important commercial food crop. But, its growth and production are significantly hampered by the bacterial pathogen pv. (Xoo) which causes leaf blight disease. Earlier studies have reported the antibacterial ability of FDA-approved niclosamide drug against Xoo. However, the underlying mechanism by which niclosamide blocks the growth of Xoo remained elusive. In the present study, by employing the microbiological, microscopical, molecular, bioinformatics and analytical tools we found that niclosamide can directly inhibit the growth of the Xoo by hampering the biofilm formation and the production of xanthomonadin and exopolysaccharide substances (EPS) required for relentless growth and virulence of Xoo. Interestingly, niclosamide was found to specifically suppress the growth of Xoo without affecting other bacteria like . Our electron microscopic observations disclosed that niclosamide disrupts the membrane permeability of Xoo and causes the release of intracellular components. Similarly, the molecular docking analysis disclosed the molecular interaction of niclosamide with the biofilm, virulence and quorum sensing related proteins, which was further substantiated by relative gene expression analysis where niclosamide was found to significantly downregulate the expression of these key regulatory genes. In addition, considerable changes in chemical structures were detected by Fourier Transform Infrared Spectroscopy (FTIR) in response to niclosamide treatment. Overall, our findings advocate the utilization of niclosamide as a safe and potent alternative antibacterial compound to control bacterial blight disease in rice.

Citrus Huanglongbing (HLB), a devastating disease caused by the unculturable bacterium ‘Candidatus Liberibacter asiaticus’ (CLas), poses a severe threat to global citrus production. CLas secretes effectors to suppress host immune responses and facilitate its colonisation. Previously, the CLas effector SECP8 (CLIBASIA₀5330) has been identified as an immune inhibitor. However, its molecular mechanisms on host immune suppression remain unclear. This study identifies the citrus transcription factor CsTCP15 as a target of SECP8. Transgenic citrus plants overexpressing CsTCP15 enhanced resistance to CLas, whereas CsTCP15‐RNAi interference plants became more susceptible, confirming its role as a positive immune regulator. Meanwhile, CsTCP15 was demonstrated to directly bind to cis‐elements of salicylic acid (SA)‐responsive genes CsPR5 and CsWRKY22, and overexpression of either gene strengthened citrus hairy roots' resistance against CLas. However, SECP8 directly interacts with CsTCP15 and inhibits its homodimerization. Concurrently, mSECP8 facilitates CsBRG3‐mediated degradation and further prevents the dimerization of CsTCP15. This two‐pronged interference eventually impairs the transcriptional activation of CsPR5 and CsWRKY22, thereby compromising salicylic acid‐mediated immunity and promoting CLas infection. Our findings reveal a virulence strategy whereby a CLas effector manipulates a key host immune regulator to establish pathogenesis.

Grape (Vitis vinifera) is susceptible to fungal pathogens and, consequently, severe yield losses. Investigating the immune mechanisms of the disease‐resistant Chinese wild grapes is crucial for developing sustainable disease resistance technologies. Here, we conducted whole‐transcriptome and methylated‐RNA‐immunoprecipitation sequencing to elucidate the immune defence mechanisms underlying grapevine responses to bacterial flagellin 22 (flg22). Certain differentially expressed miRNAs and lncRNAs responsive to flg22 showed greater differences in genotype ‘Shanyang’ than those in ‘Cabernet Sauvignon’. Functional annotation of miRNA target genes revealed that ‘Shanyang’‐specific pathways were associated with ethylene‐activated signalling, etc. Additionally, the cis‐target genes of lncRNAs were significantly enriched in the trihydroxystilbene synthase activity, etc. Notably, transient overexpression of lncRNAs TCONS_00015412, TCONS_00070812, and TCONS_00070833 in V. quinquangularis conferred significantly enhanced disease resistance compared to control plants. Significantly different m6A peaks were located in the coding sequence and stop‐codon regions. Integrated analysis of m6A and RNA‐seq suggested that m6A methylation within the coding sequence generally enhanced mRNA expression. Functional analysis further demonstrated that significantly differentially expressed genes with differential m6A modifications were enriched in the plant‐pathogen interaction pathway, etc. Furthermore, among m6A‐modified genes, LRR‐RLK in V. quinquangularis was confirmed to enhance grapevine resistance to C. diplodiella through transient overexpression. Altogether, our data strongly indicate that m6A methylation and non‐coding RNAs regulated immune‐related gene expression upon flg22 treatment, thereby modulating grapevine defence signalling pathways against pathogens. These results significantly enhance our understanding of the molecular mechanisms involving non‐coding RNAs and m6A genes in the grapevine immune‐defence responses and provide a valuable theoretical foundation for grapevine resistance breeding.

TheFusarium species Fusarium graminearum and Fusarium culmorum, which are responsible for Fusarium head blight (FHB) disease, reduce world-wide cereal crop yield and, as a consequence of their mycotoxin production in cereal grain, impact on both human and animal health. Their study is greatly promoted by the availability of the genomic sequence of F. graminearum and transcriptomic resources for both F. graminearum and its cereal hosts. Functional genomic, proteomic and metabolomic studies, in combination with targeted mutagenesis or transgenic studies, are unravelling the complex mechanisms involved in Fusarium infection, penetration and colonization of host tissues, and host avoidance thereof. This review illuminates and integrates emerging knowledge regarding the molecular crosstalk between Fusarium and its small-grain cereal hosts. An understanding of the complexity of the host-pathogen interactions will be instrumental in designing new efficient strategies for the control of FHB disease.

• Plant pathogen traits, such as transmission mode and overwintering strategy, may have important effects on dispersal and persistence, and drive disease dynamics. Still, we lack insights into how life-history traits influence spatiotemporal disease dynamics. • We adopted a multifaceted approach, combining experimental assays, theory and field surveys, to investigate whether information about two pathogen life-history traits – infectivity and overwintering strategy – can predict pathogen metapopulation dynamics in natural systems. For this, we focused on four fungal pathogens (two rust fungi, one chytrid fungus and one smut fungus) on the forest herb Anemone nemorosa. • Pathogens infecting new plants mostly via spores (the chytrid and smut fungi) had higher patch occupancies and colonization rates than pathogens causing mainly systemic infections and overwintering in the rhizomes (the two rust fungi). Although the rust fungi more often occupied well-connected plant patches, the chytrid and smut fungi were equally or more common in isolated patches. Host patch size was positively related to patch occupancy and colonization rates for all pathogens. • Predicting disease dynamics is crucial for understanding the ecological and evolutionary dynamics of host–pathogen interactions, and to prevent disease outbreaks. Our study shows that combining experiments, theory and field observations is a useful way to predict disease dynamics.

Summary Molecular changes elicited by plants in response to fungal attack and how this affects plant–pathogen interaction, including susceptibility or resistance, remain elusive. We studied the dynamics in root metabolism during compatible and incompatible interactions between chickpea and Fusarium oxysporum f. sp. ciceri (Foc), using quantitative label‐free proteomics and NMR‐based metabolomics. Results demonstrated differential expression of proteins and metabolites upon Foc inoculations in the resistant plants compared with the susceptible ones. Additionally, expression analysis of candidate genes supported the proteomic and metabolic variations in the chickpea roots upon Foc inoculation. In particular, we found that the resistant plants revealed significant increase in the carbon and nitrogen metabolism; generation of reactive oxygen species (ROS), lignification and phytoalexins. The levels of some of the pathogenesis‐related proteins were significantly higher upon Foc inoculation in the resistant plant. Interestingly, results also exhibited the crucial role of altered Yang cycle, which contributed in different methylation reactions and unfolded protein response in the chickpea roots against Foc. Overall, the observed modulations in the metabolic flux as outcome of several orchestrated molecular events are determinant of plant's role in chickpea–Foc interactions.

Tree resistance can be enhanced by a variety of biotic and abiotic inducers, including nonpathogenic and pathogenic microbes, and herbivores, resulting in enhanced protection against further biotic injury. Induced resistance (IR) could be a valuable tool in sustainable pest management. IR has been actively studied in herbaceous plant species, and, in recent years, in woody plant species, and is fast emerging as an intriguing, eco-friendly concept for enhancing tree resistance. However, before application of IR becomes possible, there is a need to increase our knowledge of the mechanisms of defence in forest trees. A richer understanding of these phenomena will play a critical role in developing sustainable integrated pest management strategies. This review summarizes our current knowledge of IR in forest trees, focusing on inducible defence mechanisms, systemic induction of resistance and phytohormone signalling networks. We conclude by discussing the potential advantages and limitations of applying IR-based management tools in forest systems.

Understanding how variation in hosts, parasites, and the environment shapes patterns of disease is key to predicting ecological and evolutionary outcomes of epidemics. Yet in spatially structured populations, variation in host resistance may be spatially confounded with variation in parasite dispersal and environmental factors that affect disease processes. To tease apart these disease drivers, we paired surveys of natural epidemics with experiments manipulating spatial variation in host susceptibility to infection. We mapped epidemics of the wind-dispersed powdery mildew pathogen Podosphaera plantaginis in five populations of its plant host, Plantago lanceolata. At 15 replicate sites within each population, we deployed groups of healthy potted ‘sentinel’ plants from five allopatric host lines. By tracking which sentinels became infected in the field and measuring pathogen connectivity and microclimate at those sites, we could test how variation in these factors affected disease when spatial variation in host resistance and soil conditions was minimized. We found that the prevalence and severity of sentinel infection varied over small spatial scales in the field populations, largely due to heterogeneity in pathogen prevalence on wild plants and unmeasured environmental factors. Microclimate was critical for disease spread only at the onset of epidemics, where humidity increased infection risk. Sentinels were more likely to become infected than initially healthy wild plants at a given field site. However, in a follow-up laboratory inoculation study we detected no significant differences between wild and sentinel plant lines in their qualitative susceptibility to pathogen isolates from the field populations, suggesting that primarily non-genetic differences between sentinel and wild hosts drove their differential infection rates in the field. Our study leverages a multi-faceted experimental approach to disentangle important biotic and abiotic drivers of disease patterns within wild populations.