Molecular plant pathology最新文献

The interaction between bacteria and filamentous phages, particularly in the context of bacterial pathogenesis, remains poorly understood compared with the well-documented interactions involving lytic phages. Here, we investigated the coevolutionary dynamics between Ralstonia pseudosolanacearum, the causative agent of plant bacterial wilt disease, and filamentous phages. Experimental coevolution revealed the critical role of the global virulence regulator PhcA in filamentous phage infection, demonstrating that its requirement for successful filamentous phage infection is independent of the type IV pili receptor. Notably, while PhcA deficiency conferred phage resistance, it did not impair filamentous phage genome replication or egress. Moreover, trade-offs between filamentous phage resistance and bacterial virulence were observed, highlighting the potential implications of filamentous phage for biocontrol strategies against R. pseudosolanacearum. Overall, our findings shed light on the intricate interplay between Ralstonia pathogens and filamentous phages, providing insights into the development of novel approaches for disease management.

Sugarcane smut, caused by Sporisorium scitamineum, is one of the most severe sugarcane diseases. A key pathogenic step is dikaryotic mycelium formation via sexual reproduction, but its regulatory mechanism is unclear. In this study, we identified a phenylacetate hydroxylase gene, SsPHACA, that is highly expressed during the sexual mating/filamentation of S. scitamineum and enriched within the phenylalanine metabolic pathway. SsPHACA deletion mutants presented significantly reduced sexual mating/filamentation and pathogenicity. Additionally, deletion of SsPHACA resulted in marked downregulation of the pheromone-responsive transcription factor gene SsPRF1, a critical regulator of sexual mating/filamentation in S. scitamineum, as well as its downstream genes at the a- and b-locus genes. Constitutive expression of SsPRF1 restored the sexual mating/filamentation of the SsPHACA deletion mutant. Metabolomic analyses revealed that SsPhacA mediates phenylalanine metabolism in S. scitamineum and modulates the accumulation of p-coumaric acid, an intermediate in phenylalanine metabolism. Exogenous supplementation with p-coumaric acid increased the transcriptional level of SsPRF1 and partially restored sexual mating/filamentation in SsPHACA deletion mutants. In summary, our results demonstrate that SsPhacA mediates the phenylalanine metabolic pathway to modulate p-coumaric acid accumulation, which increases the transcriptional level of SsPRF1, thereby regulating sexual reproduction in S. scitamineum. These findings not only identify a new regulatory factor involved in the sexual mating/filamentation of S. scitamineum, but also provide a new theoretical foundation for the development of disease control strategies targeting metabolic pathways.

The Pseudomonas syringae species complex is an important group of ubiquitous bacteria containing plant-pathogenic strains of which many strains cause damage and economic losses to a wide range of crops. Efforts to elucidate host range determinants have focused on the effector repertoires in the type 3 secretion system (T3SS). However, recently, we showed that the inability of a P. syringae pv. actinidiae strain to trigger effector-triggered immunity (ETI) in Arabidopsis thaliana is due to an inefficient T3SS and not to the absence of a recognised effector. We thus compared the T3SS efficiency of several P. syringae strains belonging to different phylogroups. We assessed the temporal dynamics of their ability to induce ion leakage, an indicator of the hypersensitive response (HR), in A. thaliana Col-0, as a proxy for T3SS function. Though not a direct measurement of T3SS efficiency, the use of a robust statistical model allowed us to reveal that P. syringae strains DC3000 avrB and M6 avrB consistently triggered a strong HR while other strains induced it at significantly different intensities depending on temperature. Among thermosensitive strains, both low and warm temperature dependencies for T3SS efficiency were observed, irrespective of their in vitro growth optimum, even among quasiclonal strains. These results reveal a strong, strain-specific regulatory role of temperature in effector injection and reinforce the importance of environmental factors in the outcome of plant-bacteria interactions. Moreover, this work highlights the need to study bacterial virulence beyond model strains such as DC3000 and B728a that are not representative of the diversity of the P. syringae species complex.

The processes of morphogenesis and differentiation are crucial for leaf development, with the duration of the morphogenetic window influencing final leaf shape. Leaves at different developmental stages exhibit distinct morphological and physiological characteristics that may influence their ability to resist pathogens, and disease resistance has been linked to developmental stage in many plant species. To understand how leaf development impacts disease resistance, we examined the immunity of leaves at distinct developmental stages, exploring the role of hormonal pathways and the impact of leaf structure and microbial interactions on disease resistance. Our findings reveal that leaves of different developmental stages exhibit distinct disease responses to various pathogens, determined primarily by the ratio between salicylic acid and jasmonic acid. Higher relative jasmonic acid content in later developing leaves was found to result in increased disease resistance to necrotrophs, while higher relative salicylic acid content in earlier developing leaves rendered them more resistant to biotrophs. This phenomenon occurred across plant ages, in several species, and also impacted the plants' response to biocontrol agents, depending on the pathway being primed. We found that structural variations among leaves can also affect disease response, due to differential recognition by the invading pathogen, and possibly also due to alterations in the leaf microbiome. Our results uncover some of the factors influencing developmental immunity in tomato, and highlight the importance of considering plant development when managing disease resistance.

Southern rice black-streaked dwarf virus (SRBSDV), transmitted by Sogatella furcifera, causes significant rice yield losses in Asia. So far, the mechanism by which SRBSDV traverses the midgut barrier to establish infection in S. furcifera midgut epithelial cells remains unknown. Here, we show that SRBSDV P10, the major outer capsid protein, enters S. furcifera midgut epithelial and haemolymph cells through interacting with the tetraspanin SfCD9 highly expressed in midgut and haemolymph cells. SfCD9 co-localises with SRBSDV P10 and relocates it from the endoplasmic reticulum (ER) to the cytomembrane of co-expressing Sf9 cells. SfCD9 localises on the cell membrane and in the cytoplasm in nonviruliferous S. furcifera midgut epithelial cells. SRBSDV P10 and SfCD9 colocalised on the midgut epithelial cell membrane of viruliferous S. furcifera at 2 days post-virus feeding (dpvf), and predominantly colocalised in epithelial cell cytoplasm at 6 dpvf. Knockdown of SfCD9 or oral delivery of the anti-SfCD9 antibody significantly inhibited SRBSDV invasion in S. furcifera. SRBSDV from infected rice crude extracts can enter SfCD9-expressing Sf9 cells, but not wild-type Sf9 cells. SfCD9 serves as a key membrane binding factor for SRBSDV entry into vector midgut epithelial cells via clathrin-mediated endocytosis. Collectively, these findings offer valuable insights into SRBSDV transmission and identify SfCD9 as a potential target to disrupt viral transmission.

The soil-dwelling bacterium Streptomyces scabiei is distributed worldwide and is the best-characterised causative agent of common scab disease, which impacts potato crops and causes significant economic losses to growers. The principal pathogenicity factor responsible for common scab development is the phytotoxin thaxtomin A, which functions as a cellulose biosynthesis inhibitor in plants. S. scabiei also produces polyketide compounds belonging to the concanamycin family, which serve as inhibitors of eukaryotic vacuolar-type ATPases and have been shown to exhibit phytotoxic activity against different plant species. It has been proposed that concanamycins contribute to the virulence of S. scabiei, but direct evidence of this has been lacking. Using constructed strains of S. scabiei that are either unable to produce concanamycins or produce elevated levels of the metabolites, we showed that concanamycins enhance the severity of disease symptoms induced by S. scabiei on radish seedlings and potato tuber tissue. We demonstrated that concanamycin production is controlled by two regulatory genes that are situated within the concanamycin biosynthetic gene cluster, and that production of concanamycins and thaxtomin A by S. scabiei is modulated by different nutritional signals. The concanamycin biosynthetic gene cluster is conserved in other common scab-causing Streptomyces spp., suggesting that these metabolites may function as important virulence determinants in multiple phytopathogenic species. Overall, this study expands our understanding of the molecular factors that enable plant host colonisation and common scab disease development by S. scabiei.

Phytocyanins (PCs) are ancient plant-specific blue copper proteins that play an important role in plant growth and development, and stress tolerance. In this study, the role of MtUC1, a member of the uclacyanin subfamily of the PC family, was analysed in the nodule symbiosis of Medicago truncatula. MtUC1 was mainly expressed in the nodule interzone and strongly induced in the later nodule developmental stage. RNA interference (RNAi) and mutation of MtUC1 led to reduced root nodule formation and degeneration of bacteroids within nodules. Cysteine protease activity in the MtUC1-RNAi inoculated roots and uc1 mutant nodules was significantly increased, the leghaemoglobin content and the expression of nitrogen-fixing enzyme genes in the uc1 mutant nodules were significantly reduced, and the nodule cells showed signs of senescence, suggesting that MtUC1 expression is required to avert nodule senescence. Transcriptomic analysis indicated that many symbiotic genes were significantly downregulated, and the senescence/defence-related genes were significantly upregulated in roots 7 days post-inoculation (dpi) and in the nodules of the uc1 mutant at 28 dpi. Yeast two-hybrid and bimolecular fluorescence complementation experiments showed that MtUC1 interacted with MtBI-1 (Bax-Inhibitor 1). Both MtUC1 and MtBI-1 were localised and co-localised to the endoplasmic reticulum and plasma membrane. In addition, MtBI-1 also showed a significantly high expression level in the mature nodules. In summary, MtUC1 may prevent the premature aging of root nodules by interacting with MtBI-1.

Pathogens secrete numerous effectors to overcome plant-derived reactive oxygen species (ROS), but how pathogens modulate effector secretion during infection remains unclear. In this study, we showed that the nucleotide diphosphate kinase Ndk1 in Fusarium graminearum plays important roles in vegetative growth, conidiation, sexual reproduction and pathogenicity. The species-specific N-terminus and three active sites of FgNdk1 functioned in the development and virulence of F. graminearum and contributed to its enzymatic activity. Protein structure results showed that the N-terminus is rich in proline, and subcellular localisation and enzymatic activity assays confirmed that it was responsible for endoplasmic reticulum (ER)-anchoring; additionally, the proline-rich feature contributed to the role of the N-terminus in enzymatic activity. We further revealed that the N-terminus of FgNdk1 exhibited a loosened structural conformation, likely facilitating the activity of FgNdk1 anchored in the ER. Moreover, FgNdk1 significantly suppressed ROS in planta. Comparative transcription analysis showed that 16 effector genes were differentially expressed in the Fgndk1 mutant, particularly during the infection stage. FgNdk1 greatly promoted the secretion of effectors FgSp10, FgSp16 and FgSp24 FgSP, which were important for the virulence of F. graminearum and ROS detoxification. Overall, FgNdk1 contributes to virulence by promoting effector secretion to scavenge ROS in planta, and its proline-rich species-specific N-terminus enhances enzymatic activity, further influencing the development and virulence of F. graminearum. These findings elucidate the mechanism by which effector secretion is modulated by an ER-anchored protein during plant fungal pathogen invasion.

Receptor-like proteins (RLPs) are cell-surface receptors that recognise pathogen- or damage-associated molecular patterns to activate immune responses, and some also participate in plant development and modulation of defence signalling. Recent advances in bioinformatics and high-throughput technologies have begun to shed light on the functional roles of RLPs, their interactions with other immune receptors, and their involvement in plant defence mechanisms. This review summarises the emerging roles of RLPs in plant immunity, with a particular focus on their dynamic interplay with receptor-like kinases (RLKs) and intracellular nucleotide-binding leucine-rich repeat receptors (NLRs) in forming integrated immune signalling networks. We also compare RLP functions across model species and major crops, revealing both conserved mechanisms and species-specific adaptations that may reflect evolutionary divergence. Furthermore, we evaluate the potential of RLPs as promising targets for disease resistance breeding. Together, this review provides a comprehensive framework for understanding RLP functions and offers strategic perspectives for leveraging RLPs in translational crop improvement.