It is demonstrated that CmVQ23 functions as a positive regulator of resistance to Verticillium dahliae by orchestrating ROS/HR-mediated cell death, antioxidant defense, phenylpropanoid pathway activation, and phytohormone signaling crosstalk, offering a promising genetic resource for improving Verticillium wilt resistance in crops.
Abstract
Verticillium dahliae is a devastating soil-borne fungal pathogen that causes severe yield losses in melon (Cucumis melo L.) and other crops. Identifying novel resistance genes is crucial for sustainable disease management. In this study, we characterized the function of CmVQ23, a candidate gene previously identified through QTL mapping, in mediating defense against V. dahliae using heterologous expression in Arabidopsis thaliana. Subcellular localization assays revealed that the CmVQ23-eGFP fusion protein predominantly localized to the nucleus, consistent with its predicted role as a co-factor of transcription factor. Upon V. dahliae inoculation, CmVQ23-overexpressing Arabidopsis lines exhibited significantly reduced disease indices and restricted fungal proliferation compared with wild-type and mutant plants, although these lines displayed altered vegetative growth, including delayed bolting and reduced plant height. Mechanistically, CmVQ23 overexpression promoted reactive oxygen species (ROS) accumulation and hypersensitive response (HR)-mediated cell death at infection sites, as evidenced by intensified DAB and trypan blue staining. Furthermore, transgenic lines maintained higher photosynthetic efficiency, enhanced antioxidant enzyme activities, and increased lignin deposition via upregulation of phenylalanine ammonia-lyase (PAL) and polyphenol oxidase (PPO). Notably, CmVQ23 overexpression markedly upregulated both salicylic acid (SA)- and jasmonic acid/ethylene (JA/ET)-responsive marker genes, including AtPR1, AtPR2, AtPR5, AtPAD4, AtPDF1.2, and AtVSP2 upon infection. Collectively, these findings demonstrate that CmVQ23 functions as a positive regulator of resistance to Verticillium dahliae by orchestrating ROS/HR-mediated cell death, antioxidant defense, phenylpropanoid pathway activation, and phytohormone signaling crosstalk, offering a promising genetic resource for improving Verticillium wilt resistance in crops.
It is demonstrated that endochitinase overexpression activates defense signaling and improves broad‐spectrum resistance, representing a promising strategy for developing disease‐resistant tomato cultivars.
Lucas José de Sousa, Ana Carolina Mendes Bezerra, Ivonaldo Reis Santos et al.· Biotechnology Journal· 0 citations
StERF87 directly activates StPR1a via GCC-box binding and integrates SA/ET signaling to enhance bacterial wilt resistance. Potato (Solanum tuberosum) is an important food crop worldwide, yet its yield is severely constrained by bacterial wilt caused by Ralstonia solanacearum. We used RNA-Seq to study gene expression in ‘Z1076-1’ at 0, 1, and 2 days post-inoculation (dpi) with R. solanacearum (10⁶ CFU mL⁻1). We identified 6663 differentially expressed genes at 1 dpi and 7390 at 2 dpi. Calcium signaling and MAPK cascade genes were upregulated at 1 dpi. PR protein and ROS-related genes showed stronger induction at 2 dpi. The ethylene-responsive transcription factor StERF87 was continuously upregulated. Its expression increased 4.7-fold at 2 dpi, with FPKM values over 100. We selected this gene for functional analysis. Transgenic potato plants overexpressing StERF87 showed lower disease severity and reduced bacterial growth in both whole plants and tuber slices. StERF87 is a transcriptional activator that directly binds the GCC-box in the StPR1a promoter to activate its transcription. After R. solanacearum inoculation, StERF87 overexpression also increased PR1b1 expression, elevated salicylic acid and ethylene levels, reduced jasmonic acid accumulation, and altered the activities of ROS-scavenging enzymes including SOD, POD, and CAT. These results show that StERF87 regulates potato defense against R. solanacearum and may be useful for breeding bacterial wilt-resistant varieties.
Ru Yu, Min Gao, Lin Cai et al.· Plant Cell Reports· 0 citations
Artificial microRNA-based gene silencing approach in PM-susceptible Vitis vinifera cv to stably silence the 'Chardonnay' ortholog of AtPMR6, VvPLL3 improves foliar resistance against the PM fungus.
Rajtilak Majumdar, H. Kaya, S. Mahanil et al.· Plant Physiology· 0 citations
The AhDef1 gene functionally validated in this study emerges as a promising candidate for engineering fungal disease resistance and aflatoxin mitigation in peanut and potentially other susceptible crops.
Nirmala Kumari Gupta, Jaykumar Patel, Gohil Mrunaliniba Yuvrajsinh et al.· Current Issues in Molecular...· 0 citations
Verticillium dahliae is a destructive soil-borne fungus with a broad host range, and its persistence in soil complicates control. Current measures, mainly resistant cultivars and chemicals, are limited and environmentally risky, promoting biocontrol as a green alternative. Here, we investigated the biocontrol mechanisms of Bacillus velezensis L33a against V. dahliae JR2 in tomato. In vitro assays on PDA plates at 26°C for 9 d showed that L33a inhibited JR2 by 58.6%, caused hyphal malformation and disruption, and its volatile organic compounds suppressed pathogen growth. In pot experiments, tomato roots dipped in JR2 suspension (1 ×10⁶ CFU/mL) for 30 min at 7 d after transplanting and grown for 21 d achieved 60.9% control efficacy. Physiological assays indicated reduced peroxidase and catalase activities, while qPCR revealed that L33a alone upregulated JA signaling (SlJAZ1, SlMYC2, SlPI II) and antioxidant (SlCAT, SlAPX) genes, with further enhancement upon JR2 co-treatment. To track their interactions, we generated GFP-labeled JR2 and RFP-labeled L33a; dual fluorescence labeling showed that L33a endophytically colonized Arabidopsis thaliana roots and competed with JR2 for the same niche, correlating with reduced pathogen colonization. Integrated metabolomic and transcriptomic analysis further revealed that L33a treatment altered pathways related to ABC transporters, amino acid metabolism, cell wall integrity, and energy metabolism in JR2, with tyrosine metabolism significantly enriched at both levels. Collectively, these findings suggest that L33a is a promising biocontrol strain for green management of tomato Verticillium wilt.
Eggplant (Solanum melongena L.) is an important solanaceous vegetable crop cultivated worldwide. Verticillium wilt, caused by Verticillium dahliae, severely restricts eggplant growth and yield, while most cultivated eggplant varieties show only limited resistance to this disease. In contrast, Solanum torvum, a wild relative of eggplant, exhibits strong natural resistance to Verticillium wilt. The molecular mechanisms underlying the contrasting responses of cultivated eggplant and S. torvum to V. dahliae infection remain poorly understood. In this study, high-throughput iTRAQ-based quantitative proteomics was used to analyze root protein profiles of S. torvum after V. dahliae inoculation. A differentially expressed protein, StoAOS1, was identified in S. torvum and was strongly induced by V. dahliae infection. StoAOS1 encodes a key enzyme in the jasmonic acid (JA) biosynthetic pathway. Further analysis showed that exogenous methyl jasmonate (MeJA) treatment markedly induced StoAOS1 expression. Virus-induced gene silencing of StoAOS1 significantly compromised Verticillium wilt resistance in S. torvum, accompanied by reduced acid-insoluble lignin accumulation and decreased transcript levels of the defense-related marker genes StoPDF1.2, StoVSP2, and StoThi2.1. Conversely, transient overexpression of StoAOS1 in Nicotiana benthamiana enhanced resistance to V. dahliae. Together, these findings suggest that StoAOS1 positively regulates Verticillium wilt resistance in S. torvum, likely through a JA-dependent defense pathway.
Yu Zhang, Lei Shen, Xu Yang et al.· Horticulturae· 0 citations
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