Molecular plant pathology最新文献

Tomato chlorosis virus (ToCV), a phloem-restricted RNA virus within the genus Crinivirus of the family Closteroviridae, exhibits a broad host range and severely impacts the yield and quality of multiple crops. Viral infection directly alters endogenous phytohormone levels, which are intricately associated with viral mobility, replication, symptom development and defence mechanisms. Previous studies have demonstrated that GATA transcription factors regulate several hormone signalling pathways in plants. In this study, we explored the interaction between ToCV p27 and SlGATA8/NbGATA11. Results indicated that ToCV p27 interacts with an 18-amino-acid at the C-terminus of SlGATA8 and NbGATA11 proteins. Silencing and overexpressing of SlGATA8 revealed its positive role in regulating tomato defence against ToCV infection. Additionally, the interaction redirected SlGATA8's subcellular localisation to plasmodesmata. Furthermore, SlGATA8 promoted the transcriptional expression of SlSnRK2 to regulate the abscisic acid (ABA) signalling pathway. In conclusion, this study confirmed that ToCV p27 impaired the transcriptional activation activity of SlGATA8 through direct interaction, thereby inhibiting the ABA pathway and ultimately facilitating viral infection. This study established a link among virus, GATA family transcription factors and phytohormones, elucidating the molecular mechanism by which ToCV-encoded p27 protein interacts with SlGATA8 to disrupt ABA balance and promote virus infection.

New outbreaks of fungal diseases are an ongoing threat to global agriculture. One known mechanism generating novel diseases is the horizontal transfer of genes between fungal species. Yet we have little understanding of how such transfers are mediated. Here, we raise the possibility that Starships, a recently discovered superfamily of giant transposable elements, might be responsible. To support this hypothesis, we discuss three potential cases where Starships may have mediated disease outbreaks. These are ToxA in wheat pathogens, genes underlying Glomerella leaf spot on apple trees, and the defoliating gene cluster of Verticillium dahliae on cotton. In the Verticillium example, we provide strong evidence for a Starship-mediated mechanism: disease-promoting genes reside in closely related Starships across distantly related species. We aim to spark interest in Starships' roles in fungal pathogens and how this knowledge could inform disease management strategies.

Pseudomonas syringae pathovar aesculi (E-Pae) causes bleeding canker disease in the woody tissue of European horse chestnut (HC). Comparative genomic analysis of E-Pae with a related leaf-infecting strain (I-Pae) and other P. syringae strains identified candidate virulence genes for colonisation of woody tissue, including a sucrose uptake and utilisation system (scrYABCDBR cluster) found in 162 of 206 P. syringae strains spanning the pangenome. Growth analysis using sucrose as sole carbon source showed that I-Pae (lacking the gene cluster) was unable to grow whereas E-Pae could grow. P. savastanoi pv. phaseolicola 1448A and P. syringae pv. morsprunorum R15244 were compromised in growth despite the presence of the gene cluster. Sucrose utilisation assays using scrB and scrY mutants and complemented strains confirmed the importance of the cluster for sucrose metabolism in vitro. Pathogenicity assays in HC revealed the sucrose gene cluster is important for symptom development in the woody tissue. While the scr genes contribute to disease causation, they were not essential for pathogen fitness when compared to hrpL and hopAB1 mutants. E-Pae caused disease symptoms in HC leaves, suggesting the strain has the potential to infect leaves as well. However, it was notable that the scrB mutant of E-Pae caused increased disease symptoms, possibly highlighting a niche adaptation strategy for I-Pae to cause leaf spots in HC as well as constraining E-Pae to predominantly infect the woody tissue.

Stylosanthes spp. (stylo) is an important leguminous forage cultivated in tropical areas. Anthracnose caused by Colletotrichum gloeosporioides is a destructive disease that limits the yield of stylo. Therefore, improving the resistance of stylo is crucial to control stylo anthracnose. In this study, the resistance evaluation of 40 Chinese stylo accessions was performed, including the main cultivar Stylosanthes guianensis 'Reyan No. 2' (RY2) as a susceptible control. Twelve stylo accessions were rated as highly resistant, with 2001-84 showing the strongest resistance. Compared to RY2, 2001-84 exhibited significantly milder disease symptoms, slower fungal colonisation, and higher pathogen-induced antioxidant enzyme activities. Integrated phosphoproteomics and plasma membrane (PM) enriched proteomics of both RY2 and 2001-84 revealed that pathogen-responsive proteins were predominantly associated with kinase signalling, transport processes, and oxidoreductase activity. A PM-localised E3 ubiquitin ligase, SgATL31, was identified as increasing in response to pathogen in both proteomic analyses. Functional characterisation demonstrated that SgATL31 overexpression in Arabidopsis enhanced resistance to C. gloeosporioides, promoted chitin-induced reactive oxygen species (ROS) production in both Arabidopsis and stylo protoplasts, and increased antioxidant enzyme activities following pathogen infection. Furthermore, the expression levels of SgATL31 were induced by pathogen infection in all 40 stylo accessions and accumulated to higher levels in resistant accessions. Overall, our findings not only identify 2001-84 as a valuable genetic resource for anthracnose resistance but also establish SgATL31 as a regulator of plant immunity against anthracnose, potentially through modulation of ROS and antioxidant pathways, providing important insights for improving disease resistance in stylo.

Plant pathogens infect hosts through sophisticated molecular strategies, with N-glycosylation serving as a critical post-translational modification that regulates their virulence. This review comprehensively summarises and discusses the role of N-glycosylation in regulating potential pathogenic mechanisms, including fungal growth and development, cell wall integrity, infection structures (e.g., appressoria, invasive hyphae) and the secretion of effector proteins. By ensuring proper protein folding, stability and interaction with host defences, N-glycosylation enables pathogens to evade plant immune recognition, such as pathogen-associated molecular pattern (PAMP)-triggered immunity, and establish successful infections. Advances in glycomic techniques and proteomics offer tools to dissect these mechanisms with enhanced precision. Future research directions regarding N-glycosylation in plant pathogens should emphasise the development of small-molecule targeted drugs against pathogens and the creation of enzyme inhibitors to disrupt virulence factors. This work provides a perspective for further study regarding N-glycosylation in the plant-pathogenic mechanisms and effective disease control.

Pectobacterium actinidiae is one of the primary pathogens that causes summer canker disease in kiwifruit, yet its pathogenic mechanisms remain unknown. The exopolysaccharide PCAP-1a, isolated from the fermentation broth of P. actinidiae strain GX1, exhibits notable cytotoxicity and acts as a virulence factor facilitating host infection. Genome-wide analysis revealed a 21-gene cluster responsible for the biosynthesis of exopolysaccharides in GX1. Homologous recombination was used to systematically knock out these genes, which led to the identification of RmlA as a key protein in the synthesis of the PCAP-1a precursor. The deletion of the rmlA gene significantly affected the yield of PCAP-1a and resulted in a direct reduction in GX1 pathogenicity. Further studies revealed that mutations in the substrate binding site of RmlA weakened its capacity to bind G-1-P and dTTP, which led to markedly reduced pathogenicity in the corresponding complemented strains. This study indicates that the exopolysaccharide PCAP-1a serves as a virulence factor in the pathogenesis of GX1, and its biosynthesis depends on the polysaccharide synthesis gene rmlA and the substrate binding activity of its encoded protein.

Acidovorax citrulli, the causal pathogen of bacterial fruit blotch of cucurbits, relies on a functional type III secretion system (T3SS) for pathogenicity. Two-component systems (TCSs) are primary signal transduction mechanisms for bacteria to detect and adapt to various environmental conditions. However, the role of TCS on regulating T3SS and other virulence factors in response to environmental stimuli is still poorly understood in A. citrulli. Here, we report the identification of a conserved TCS, OmpR/EnvZ, involved in hypersensitive response (HR) induction in Nicotiana benthamiana by screening a transposon-insertion library in the group II strain xjL12 of A. citrulli. Transcription analysis confirmed that OmpR_Ac/EnvZ_Ac was upregulated in response to elevated osmotic pressure, low and high pH conditions, and host environment. Deletions of envZ_Ac, ompR_Ac, or both envZ_Ac and ompR_Ac in A. citrulli attenuated virulence to melon seedlings and mature leaf tissues, and delayed HR in N. benthamiana. OmpR_Ac was activated by EnvZ_Ac and directly bound to the promoter region of hrpG, a major regulator of T3SS. This binding activated hrpG transcription and promoted T3SS assembly in T3SS-inducing medium, XVM2. Additionally, the OmpR_Ac/EnvZ_Ac mutants of A. citrulli displayed reduced swimming motility due to impaired flagella formation, but also had enhanced biofilm formation and exopolysaccharide production. OmpR_Ac/EnvZ_Ac regulation of these virulence factors in A. citrulli depended on its own conserved phosphorylation sites. This work illuminates a signalling pathway for regulating the T3SS and provides insights into the OmpR/EnvZ-mediated virulence regulatory network in A. citrulli.

Western flower thrips (Frankliniella occidentalis) are among the most significant invasive pests worldwide. In addition to causing direct plant damage, they transmit tomato spotted wilt virus (TSWV) (species Orthotospovirus tomatomaculae; genus Orthotospovirus), a member of the genus Orthotospovirus. Although numerous studies have examined virus-insect-host plant interactions, research on the TSWV-thrips-plant tripartite interaction remains limited. In this study, we found that F. occidentalis can induce plant defence responses. FoCSP1, a chemosensory protein from F. occidentalis, was identified as a salivary elicitor capable of inducing serial plant defence responses in Nicotiana benthamiana. Our results revealed that the FoCSP1-induced plant defence responses did not affect thrips feeding preference but significantly inhibited both offspring and egg production. Moreover, TSWV impairs these defence responses through its encoded proteins, N and NSs, thereby alleviating the FoCSP1-mediated suppression of thrips offspring and egg production. Collectively, these findings indicate that TSWV promotes the offspring and egg production of its thrips vector by inhibiting plant defences induced by FoCSP1, providing new insights into the TSWV-thrips-plant tripartite interaction.

Alternaria solani is an important necrotrophic pathogen causing potato early blight. However, the pathogenic molecular mechanisms of A. solani remain unclear. Previous work identified a specific effector AsCEP20 in A. solani through multi-omics analysis. AsCEP20 is required for the full virulence of A. solani and targets the host chloroplasts. In this study, we screened out 46 candidate proteins that potentially interact with AsCEP20 in Nicotiana benthamiana using co-immunoprecipitation followed by liquid chromatography-tandem mass spectrometry analysis. We identified a candidate target protein in potato, filamentation temperature-sensitive H4 (StFtsH4), which is located in chloroplasts, based on homologous alignment and subcellular localisation analysis. The interaction between AsCEP20 and StFtsH4 was further confirmed by co-immunoprecipitation, yeast two-hybrid assay and bimolecular fluorescence complementation assays. The interaction site between AsCEP20 and StFtsH4 is also the chloroplast. Silencing the potato StFtsH4 gene resulted in suppressed pathogen-associated molecular pattern-triggered reactive oxygen species (ROS) bursts, and defence-related genes were significantly downregulated. These results suggest that StFtsH4 positively regulates plant immunity. Therefore, AsCEP20 targets the chloroplast protein StFtsH4 to promote pathogen infection. AsCEP20 attenuates the efficiency of light energy utilisation in photosynthesis by targeting StFtsH4. These results suggest that AsCEP20 suppresses StFtsH4-mediated potato disease resistance to A. solani. With the increase of light intensity, ROS continued to accumulate in the chloroplast of StFtsH4-silenced plant leaves, while defence-related genes significantly decreased. Our findings reveal that the impaired StFtsH4 function limits plant photosynthesis, thereby affecting immune signalling.

Colletotrichum gloeosporioides is a major agricultural pathogen of crops that has also been identified as an endophyte of the medicinal plant Huperzia serrata. Both H. serrata and C. gloeosporioides produce huperzine A, a potential treatment for Alzheimer's disease. In this study, a nonpathogenic C. gloeosporioides strain (NWUHS001) was isolated and its genome sequenced. Gene structure prediction identified 15,413 protein-coding genes and 879 noncoding RNAs. Through PHI-base database prediction, we found that NWUHS001 lacks two key pathogenicity genes CgDN3 and cap20, which may be the cause of its nonpathogenicity. Comparative genomic analysis showed that the number of genes encoding pectin lyase B (pelB), pectin lyase (pnl) and polygalacturonase (pg) in NWUHS001 was significantly lower than that in pathogenic strains during the expansion of mycelium into host tissues. This caused slow growth and incapability to penetrate host cells. In contrast, in NWUHS001, genes involved in carbon acquisition such as ribose and amino sugar metabolic pathways were enriched, indicating active metabolite exchange with the host. In addition, by comparing the genome of NWUHS001 with that of the host H. serrata, we found that polyketosynthetase (pksIII), a key gene in the host huperzine A biosynthetic pathway, may possibly have been acquired from the fungus by horizontal gene transfer (HGT). This study explained the possible genetic evolution mechanism of C. gloeosporioides from pathogenicity to nonpathogenicity, which is of value for studying the interaction between microorganisms and plants. It also provided clues to the genetic evolution of the biosynthetic pathway of huperzine A.