ABSTRACT Panax notoginseng is an edible traditional medicinal plant, but it is highly susceptible to Panax notoginseng virus Y (PnVY). This study revealed that salicylic acid (SA) treatment decreases this susceptibility. The underlying molecular mechanism was elucidated by integrating physiological, multi‐omics and genetic approaches. SA application alleviated PnVY‐induced photosynthetic inhibition and activated antioxidant enzymes, thereby decreasing reactive oxygen species levels and maintaining redox homeostasis. Upon PnVY inoculation, SA triggered a range of defence responses. The exogenous application of SA promoted the accumulation of phenylpropanoids, alkaloids and flavonoids, which was consistent with the upregulated expression of phenylpropanoid biosynthesis‐related genes. Transcriptional regulatory network analysis revealed that the ethylene‐responsive transcription factor PnERF120 may positively regulate the biosynthesis of phenolic acids including SA. Overexpressing PnERF120 enhanced the resistance of P. notoginseng to PnVY, activated SA biosynthesis and signal transduction pathway, upregulated the RNA‐silencing‐related genes and improved phenolic acid accumulation. However, silencing PnERF120 in P. notoginseng had the opposite effect. Additionally, yeast one‐hybrid and dual‐luciferase assays indicated that PnERF120 binds to the promoter of PnPAL1 and activates PnPAL1 expression. In conclusion, PnERF120 positively regulates defence against PnVY infection by modulating SA biosynthesis and the SA signalling pathway.
ABSTRACT Taxonomy Bacteria; Proteobacteria , gamma subdivision; Order Pseudomonadales ; Family Pseudomonadaceae ; Genus Pseudomonas ; Pseudomonas avellanae species complex, which includes different pathogenic lineages previously classified within the P. syringae complex, namely the pathovars avellanae , theae , actinidiae , and morsprunorum race 2. Microbiological Properties As a whole, the P. avellanae species complex genome comprises 19.4% conserved genes and 80.6% flexible genome. Mobile genetic elements are present within the complex. Strains associated with bacterial canker of European hazelnut possess two plasmids, whereas multiple plasmids and megaplasmids can occur in the lineages associated with bacterial canker of kiwifruit and cherry. Fourteen type III secretion system effectors are shared by all lineages of the species, and each lineage apparently possesses specific effector proteins. Phytotoxins, such as phaseolotoxin, coronatine, and tabtoxin, can be produced by some lineages of P. avellanae . Siderophores are present in the P. avellanae species complex. Host Range Corylus avellana , Camellia sinensis var. sinensis , Actinidia chinensis var. chinensis , A. chinensis var. deliciosa , Prunus avium , P. cerasus , P. domestica . A strain of P. avellanae has also been isolated from river epilithon. Disease Symptoms Pseudomonas avellanae can cause severe symptoms, including bud necrosis (kiwifruit), leaf necrosis and wilting (hazelnut, tea, kiwifruit, cherry/plum), shoot and twig blight (hazelnut, tea, kiwifruit, cherry/plum), flower necrosis (kiwifruit), fruit necrosis (cherry/plum), trunk canker (hazelnut, kiwifruit, cherry/plum), and plant death (hazelnut, tea, kiwifruit). Epidemiology Some P. avellanae lineages are favoured by air temperatures below 0°C. Penetration mainly occurs through stomata, leaf scars, and wounds induced by frost events. P. avellanae species complex exhibits both epiphytic and endophytic phases. During summer, very high temperatures can reduce the multiplication and dispersal of the pathogen. The global circulation of latently infected propagative plant material largely favours the spread of P. avellanae lineages across different cultivation areas. Detection Pathogens belonging to this complex can be detected in both symptomatic and asymptomatic plant tissues (e.g., twigs, buds, and cankers) using various conventional techniques and molecular tools (standard‐, duplex‐, TaqMan‐, real‐time PCR, LAMP, MLSA). Depending on the targeted symptoms, pathogenicity tests may be conducted on leaf, leaf scars or woody tissues. Disease Control Disease management is based on spray treatments to the crown using copper compounds applied in spring and autumn, as well as after harvest, during leaf fall, and following hail, frost events, and pruning. Balanced plant nutrition is important to reduce the risk of severe infection. Alternative promising strategies include the application of biocontrol agents, natural products, and bacteriophages.
ABSTRACT Rice foot rot, caused by Dickeya oryzae , is a destructive bacterial disease. The Vfm quorum‐sensing (QS) system is a key virulence regulator of this pathogen. However, the mechanisms by which it perceives and integrates upstream environmental signals for precise transcriptional control are poorly understood. Here, we identify a cascade regulatory network involving the MarR‐family transcription factors OhrR and EmrR. Deletion of ohrR in D. oryzae EC1 significantly reduced the Vfm signalling activity, diminished the production of virulence factors including phytotoxin zeamines and plant cell wall‐degrading enzymes, and attenuated its pathogenicity. Molecular analyses revealed that OhrR directly bound to the key promoters in the vfm cluster (P vfmA , P vfmK , P vfmE and P vfmF ) and activated their transcription. Intriguingly, OhrR also directly activated the expression of emrR , which encodes another MarR‐family transcriptional regulator. In contrast to the activator role of OhrR, EmrR acted as a feedback inhibitor, directly bound to the same vfm promoter regions but repressed their transcription. OhrR–EmrR thus acts as a two‐tiered ‘activation–inhibition’ regulatory circuit in modulation of the Vfm QS system, in which OhrR functions as a master switch for environmental signal response and initiation of the Vfm system, whereas EmrR acts as a precise brake to prevent overexpression of virulence determinants. The findings from this study unveil the fascinating interaction between OhrR–EmrR and the Vfm QS system, and depict a novel mechanism for precise virulence control in D. oryzae via complex, dynamic transcriptional reprogramming.
ABSTRACT Botrytis cinerea triggers destructive grey mould with substantial economic losses, yet the functions of numerous pathogenicity genes remain largely unclear. Here, by screening a T‐DNA insertion library, we identified BcARS2 , a key component of the Microprocessor complex. BcARS2 is constitutively expressed, localizes to the nucleus, and modulates gene expression. The Δ Bcars2 mutants exhibited impaired vegetative growth, enhanced conidiophore sporulation, increased conidiation, reduced sclerotial size, and increased sensitivity to multiple stresses. Pathogenicity assays showed that different inoculation methods led to distinct virulence phenotypes in Δ Bcars2 mutants. Microscopic observations revealed that although the Δ Bcars2 mutant formed normal appressoria and successfully invaded host cells, its invasive hyphae exhibited limited expansion. Furthermore, exogenous cAMP did not restore the impaired development of infection cushions (ICs), resulting in defective infection. Multitranscriptome analyses demonstrated that BcARS2 positively regulates BcPDI1 and BcCGF1 , two key genes responsible for reactive oxygen species (ROS) homeostasis and highly expressed during the IC developmental stage. Correspondingly, deletion of BcARS2 upregulated catalase gene expression, elevated catalase activity, reduced H 2 O 2 accumulation, disturbed ROS balance, and ultimately inhibited IC formation. In addition, most toxin biosynthesis‐related genes, which are normally upregulated during IC development, were significantly downregulated in the Δ Bcars2 mutant. Collectively, BcARS2 modulates the virulence of B. cinerea by regulating IC development, vegetative hyphal growth, and stress responses.
Coffee leaf rust, caused by the obligate biotrophic fungus Hemileia vastatrix, remains the most destructive disease of coffee worldwide. Although genomic and transcriptomic studies have identified a large number of candidate effectors, experimental evidence supporting their biological roles during infection remains limited. Here, we integrated functional assays, temporal expression profiling during coffee infection and subcellular localization analyses to investigate the biological properties of 44 H. vastatrix effector candidates (HvECs). Using the Pseudomonas fluorescens EtHAn effector delivery system in Nicotiana benthamiana, 15 HvECs consistently suppressed pattern-triggered immunity (PTI), indicating that immune suppression is a widespread property among the H. vastatrix effector repertoire, as assessed in this heterologous system. Five HvECs also attenuated AvrB-triggered effector-triggered immunity (ETI), and three suppressed both PTI and ETI, suggesting that a subset of HvECs targets conserved regulatory nodes shared by these interconnected immune pathways. Temporal expression profiling revealed sequential deployment of HvECs throughout infection, with distinct subsets predominating during pre-biotrophic development, host penetration or biotrophic colonization, consistent with stage-specific functions during fungal pathogenesis. Subcellular localization analyses further showed that HvECs preferentially accumulated in the nucleus or chloroplasts, compartments known as central hubs of plant immune regulation. This study provides the most comprehensive functional characterization of H. vastatrix effector candidates to date, establishes a biologically informed framework for prioritizing candidates for future identification of avirulence determinants recognized by SH resistance genes, and advances our understanding of how the coffee rust fungus orchestrates immune suppression across time and cellular space during pathogenesis.
