ArticleBMC genomics2026
VDAL enhances wheat resistance to Fusarium graminearum by modulating defense signaling and reducing deoxynivalenol accumulation.
Article in BMC genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a destructive disease leading to significant yield losses and mycotoxin contamination worldwide. This study investigated the efficacy and molecular mechanism of VDAL (Verticillium dahliae Asp-f2 Like protein), a novel plant immune inducer, in enhancing wheat resistance to F. graminearum. Field trials over two consecutive seasons revealed that three applications of VDAL effectively reduced both disease severity (by > 65%) and deoxynivalenol (DON) accumulation in wheat grains. In vitro assays confirmed that VDAL does not directly inhibit fungal growth. Transcriptomic and qPCR analysis indicated that VDAL's protection is associated with reduced expression of specific fungal trichothecene biosynthesis genes (TRI9, TRI12) during infection. Strikingly, VDAL orchestrated distinct wheat transcriptional responses conditional on the presence of the pathogen. Under pathogen-free conditions, VDAL enhanced defenses by upregulating genes involved in cuticular wax biosynthesis, flavonoids and terpenoids biosynthesis, and photosynthetic capacity, thereby reinforcing physical and chemical barriers. Upon F. graminearum challenge, VDAL specifically activated a broad-spectrum immune response, including genes associated with pattern-triggered immunity (PTI), salicylic acid (SA)/jasmonic acid (JA)/ethylene (ET) signaling, reactive oxygen species (ROS) generation, calcium flux, cell wall proteins, fungal resistance genes, and systemic acquired resistance (SAR). Importantly, this immune activation remained sustained for at least five days post-application. Key transcription factors integrating hormone signaling (WRKY70, MYB44, TIFY11, ERFs) were identified as central regulators in this process. Our findings indicate that VDAL enhances resistance to FHB by activating sustained host defense responses. The pathogen-dependent induction of defense pathways highlights the precision and efficiency of immune modulation underscores VDAL's potential as a sustainable biocontrol agent for integrated FHB management.
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