Molecular plant pathology最新文献

Tomato yellow leaf curl Guangdong virus (TYLCGdV), a monopartite begomovirus first identified in 2004, remains poorly characterised. In this study, we demonstrate that TYLCGdV associates with a betasatellite, TYLCGdB, and the βC1 protein encoded by TYLCGdB is essential for symptom development. We also explore the role of TYLCGdV C4 protein by generating a C4-deficient infectious clone (TYLCGdV_mC4), revealing a dynamic role for TYLCGdV C4. Specifically, viral accumulation in TYLCGdV_mC4/TYLCGdB-inoculated plants was significantly lower than that in TYLCGdV/TYLCGdB-inoculated plants at 7 and 14 days post-inoculation (dpi), but surpassed that of TYLCGdV/TYLCGdB-inoculated plants by 25 dpi. Furthermore, although C4 proteins in other begomoviruses typically exhibit one or more of the following properties: (i) suppression of post-transcriptional gene silencing (PTGS), (ii) suppression of transcriptional gene silencing (TGS), (iii) enhancement of pathogenicity in potato virus X (PVX) and (iv) symptom induction when transgenically expressed, TYLCGdV C4 did not exhibit any of these properties. However, the dynamic role of TYLCGdV C4 in viral infection appears to result from its effects on viral DNA methylation. At 7 dpi, the cytosine methylation level in the TYLCGdVmC4 genome was notably elevated compared to that of the wild-type virus. However, this trend reversed by 14 dpi, with the wild-type virus exhibiting a higher methylation level. By 25 dpi, the cytosine methylation levels of both TYLCGdVmC4 and TYLCGdV were comparable. These results indicate that TYLCGdV C4 modulates viral infection via an unconventional mechanism. This novel observation highlights the need for further investigation into the diverse roles of C4 proteins in begomoviruses.

Two phylogenetically unrelated viruses transmitted by different insect vectors, tomato spotted wilt virus (TSWV) and tomato yellow leaf curl virus (TYLCV), are major threats to tomato and other vegetable production. Although co-infections of TSWV and TYLCV on the same host plant have been reported on numerous occasions, there is still lack of research attempting to elucidate the mechanisms underlying the relationship between two viruses when they coexist in the same tomato or other plants. After assessing the effect of four TSWV-coded proteins on suppressing TYLCV in TSWV N transgenic Nicotiana benthamiana seedlings, the TSWV N protein proved to be effective in reducing TYLCV quantity and viral symptoms. Western blot analysis indicated that TSWV N was involved in down-regulating the expression level of the V1, C3, and C4 proteins of TYLCV, among which V1 was the most significantly suppressed one. Moreover, TSWV N was confirmed to reduce TYLCV V1 within both nucleus and cytoplasm, but a greater suppression was observed in cytoplasm. The co-immunoprecipitation and mass spectrometry identified 244 differential proteins from the TYLCV-infected TSWV N transgenic N. benthamiana seedling. These proteins pertaining to energy metabolism pathways were enriched, suggesting that TSWV N could inhibit TYLCV through competing for energy or regulating energy-related metabolism. The evidence presented here offers a novel perspective that will facilitate a comprehensive understanding of virus-virus and virus-host interactions, as well as a potential strategy for plant virus control through using TSWV N in the near future.

Apple bitter rot is caused by various Colletotrichum spp. that threaten apple production globally resulting in millions of dollars in damage annually. The fungus causes a decline in fruit quality and yield, eventually rotting the fruit and rendering it inedible. The pathogen is difficult to keep out of orchards because of its broad host range and transmissibility by rain splash and insects. Once the disease manifests, pathogen identification is difficult due to evolving taxonomy and similar morphology between species. Current management strategies are threatened by an increase in fungicide resistance and regulations on many multisite fungicides, leading to a pressing need for new management options for control. This review aims to summarise the most current knowledge regarding the biology, virulence factors, ecology, omics and emerging management strategies for Colletotrichum species that cause apple bitter rot.

Taxonomy: Colletotrichum species-Domain Eukaryota, Kingdom Fungi, Phylum Ascomycota, Class Sordariomycetes, Order Glomerellales, Family Glomerellaceae, Genus Colletotrichum.

Biology: Hemibiotrophic pathogen with a wide host range that establishes a biotrophic interaction where it penetrates host plants using appressoria followed by a switch to necrotrophy causing rot symptoms.

Toxins: Cercosporin, colletotrichins, colletotric acid, ferricrocin.

Host range: The host range varies by species but largely occurs on dicotyledonous plants and is less prevalent on monocots as well as gymnosperms, ferns, mosses and animals (e.g., insects).

Disease symptoms: Symptoms often manifest as flat to sunken necrotic areas on fruit. Lesions on leaves and fruit can have concentric rings with abundant pathogen sporulation.

Disease control: Colletotrichum spp. are primarily managed by single-site quinone outside inhibitor (Qol), methyl benzimidazole carbamate (MBC), demethylation inhibitor (DMI) fungicides, and multisite dithiocarbamate and phthalimide fungicides. Susceptibility may vary with species, strain specificity, or geographic region. Other management options include clean stock production, cultural practices, resistance breeding, and biological control through the introduction of protective or competing microorganisms.

The begomoviral V2 protein is known to be multifunctional, including its interaction with and inhibition of CYP1, a papain-like cysteine protease (PLCP). However, the effect of this interaction on viral pathogenicity remains unclear. Cotton leaf curl Multan virus (CLCuMuV), a typical monopartite begomovirus associated with a betasatellite, is one of the main pathogens responsible for cotton leaf curl disease. This study verifies the interaction between CLCuMuV V2 and NbCP15, a PLCP homologue in Nicotiana benthamiana. The results show that V2 can be cleaved by NbCP15 in vitro, with the N-terminal cleavage site located between the second and third amino acids. Using an Agrobacterium-mediated inoculation method, we investigated the influence of cleavage sites on viral pathogenicity. The findings indicate that mutation of the third amino acid in V2 (V2^D3A) reduced the pathogenicity of both heterologous PVX and CLCuMuV. Additionally, the NbCP15 gene mutation in N. benthamiana (nbcp15) also resulted in reduced CLCuMuV pathogenicity. These results suggest that CLCuMuV V2 may promote viral infection through its interaction with plant PLCPs.

Autophagy, one of the most widespread and highly conserved protein degradation systems in eukaryotic cells, plays an important role in plant growth, development and stress response. Beclin 1 is a core component of the phosphatidylinositol 3-kinase (PI3K) autophagy complex and positively regulates plant immunity against viruses. The upregulation of Eureka lemon ClBeclin1 was observed in response to citrus yellow vein clearing virus (CYVCV) infection. However, the function of ClBeclin1 and the underlying mechanism during CYVCV colonisation remain unclear. Here, the resistance evaluation of the overexpression and silencing of ClBeclin1 in Eureka lemon hairy roots revealed it as a positive regulator of citrus immunity against CYVCV. Transcriptomic profiling and metabolic analyses along with genetic evidence implied that the overexpression of ClBeclin1 positively triggered reactive oxygen species (ROS)- and jasmonic acid (JA)-mediated immunity in citrus. The accumulation of ROS and JA contents was attributed to the autophagic degradation of the ROS scavenger ClAPX1 via ClBeclin1 overexpression. Exogenous application of either H₂O₂ or JA significantly reduced CYVCV colonisation and vein-clearing symptoms on the host. Collectively, our findings indicate that ClBeclin1 activation contributes to citrus immunity against CYVCV through triggering ROS- and JA-mediated defence responses, and the accumulation of ROS and JA resulted from the autophagic degradation of ClAPX1 by ClBeclin1.

Fungal plant pathogens cause major crop losses worldwide, with many featuring compartmentalised genomes that include both core and accessory regions, which are believed to drive adaptation. The highly host-specific fungus Colletotrichum lupini greatly impacts lupin (Lupinus spp.) cultivation. This pathogen is part of clade 1 of the C. acutatum species complex and comprises four genetically uniform, presumably clonal, lineages (I-IV). Despite this, variation in virulence and morphology has been observed within these lineages. To investigate the potential sources of genetic variability in this asexual fungus, we compared the genomes of 16 C. lupini strains and 17 related Colletotrichum species. Phylogenomics confirmed the presence of four distinct lineages, but further examination based on genome size, gene content, transposable elements (TEs), and deletions revealed that lineage II could be split into two groups, II-A and II-B. TE content varied between lineages and correlated strongly with genome size variation, supporting a role for TEs in genome expansion in this species. Pangenome analysis revealed a highly variable accessory genome, including a minichromosome present in lineages II, III, and IV, but absent in lineage I. Accessory genes and effectors appeared to cluster in proximity to TEs. Presence/absence variation of putative effectors was lineage-specific, suggesting that these genes play a crucial role in determining host range. Notably, no effectors were found on the TE-rich minichromosome. Our findings shed light on the potential mechanisms generating genetic diversity in this asexual fungal pathogen that could aid future disease management.

Many gram-negative pathogenic bacteria use type III effector proteins (T3Es) as essential virulence factors to suppress host immunity and to cause disease. However, in many cases the molecular function of T3Es remains unknown. The plant pathogen Xanthomonas campestris pv. vesicatoria (Xcv) is the causal agent of bacterial spot disease on tomato and pepper plants and is known to translocate around 36 T3Es into its host cell, which collectively suppress plant defence and promote infection. XopM is an Xcv core T3E with unknown function that has no similarity to any other known protein. We found that XopM interacts with vesicle-associated membrane protein (VAMP)-associated proteins (VAPs) in an isoform-specific manner. The endoplasmic reticulum (ER) integral membrane protein VAP is a common component of membrane contact sites involved in both tethering and lipid transfer by binding directly to proteins containing an FFAT (two phenylalanines [FF] in an acidic tract [AT]) motif. Sequence analyses revealed that XopM displays two FFAT motifs that cooperatively mediated the interaction of XopM with VAP. When expressed in plants, XopM supported growth of a nonpathogenic bacterial strain and dampened the production of reactive oxygen species, indicating its ability to suppress plant immunity. Further analyses revealed that the interaction with VAP and the ability to suppress microbe-associated molecular pattern-triggered immunity (MTI) are structurally and functionally separable, although XopM requires localisation to the host membrane system for full MTI suppression activity. We discuss a working model in which XopM uses FFAT motifs to target the membrane to interfere with early MTI responses.

Microbial pathogens and other parasites can modify the development of their hosts, either as a target or a side effect of their virulence activities. The plant-pathogenic bacterium Ralstonia solanacearum, causal agent of the devastating bacterial wilt disease, is a soilborne microbe that invades host plants through their roots and later proliferates in xylem vessels. In this work, we studied the early stages of R. solanacearum infection in the model plant Arabidopsis thaliana, using an in vitro infection system. In addition to the previously reported inhibition of primary root length and increase in root hair formation at the root tip, we observed an earlier xylem differentiation during R. solanacearum infection that occurs in a HrpG-dependent manner, suggesting that the pathogen actively promotes the development of the vascular system upon invasion of the root. Moreover, we found that the phytohormone auxin, of which the accumulation is promoted by the bacterial infection, is required for the R. solanacearum-triggered induction of root hair formation but not earlier xylem differentiation. Altogether, our results shed light on the capacity of R. solanacearum to induce alterations of root developmental pathways and on the role of auxin in this process.

Zhu, L.-J., Zhu, Y., Zou, C., Su, L.-Y., Zhang, C.-T., Wang, C. et al. (2024) New persistent plant RNA virus carries mutations to weaken viral suppression of antiviral RNA interference. Molecular Plant Pathology, 25, e70020. Available from: https://doi.org/10.1111/mpp.70020 The following errors have been identified in the above published article: The co-first authors and co-corresponding authors are not indicated. The order of the funds appearing in the Funding information of the article are not consistent with the order in the Acknowledgements. The authors would like to correct these errors as follows: Li-Juan Zhu and Yu Zhu contributed equally to this work. Jian-Guo Wu and Yan-Hong Han are co-corresponding authors. Jiang-Guo Wu: wujianguo81@126.com; Yan-Hong Han: yan-hong@fafu.edu The correct order of funds is: National Natural Science Foundation of China, Grant/Award Number 32025031 and 31,900,153, National Key Research and Development Program of China, Grant/Award Number 2023YFF1000500 and Special Fund Project for Science and Technology Innovation of FAFU, Grant/Award Number KFB23013. We apologise for these errors.

The organs of a plant species vary in cell structure, metabolism and defence responses. However, the mechanisms that enable a single pathogen to colonise different plant organs remain unclear. Here we compared the transcriptome of the oomycete pathogen Phytophthora sojae during infection of roots versus leaves of soybeans. We found differences in the transcript levels of hundreds of pathogenicity-related genes, particularly genes encoding carbohydrate-active enzymes, secreted (effector) proteins, oxidoreductase-related proteins and transporters. To identify the key regulator for root-specific infection, we knocked out root-specific transcription factors (TFs) and found the mutants of PsBZPc29, which encodes a member of an oomycete-specific class of basic leucine zipper (bZIP) TFs, displayed reduced virulence on soybean roots but not on leaves. More than 60% of the root-specific genes showed reduced expression in the mutants during root infection. The results suggest that transcriptional regulation underlies the organ-specific infection by P. sojae, and that a bZIP TF plays a key role in root-specific transcriptional regulation.