Fusarium head blight (FHB) is a devastating disease that poses a significant threat to the global wheat production industry. However, there is a limited pool of genes available for genetic enhancement of wheat resistance to FHB, and the mechanism underlying the disease resistance is not yet fully understood. Our previous study identified a late embryogenesis abundant protein, encoded by TaG3LEA-25, which was specifically accumulated in the FHB-resistant wheat varieties. In the current work, the overexpression of TaG3LEA-25 in wheat significantly enhanced resistance to FHB. TaG3LEA-25 may mediate FHB resistance by maintaining the integrity of plant cell, which was supported by our established wheat protoplast-F. graminearum interaction system and by the experimental evidence that it interacts with tubulin. A single nucleotide polymorphism (SNP) variation in the promoter of TaG3LEA-25 is within the cis-element for MYC2, and correlated significantly with FHB resistance in a panel of breeding varieties. Varieties carrying contrasting alleles at the SNP showed differential responses to jasmonic acid and exhibited distinct phenotypic responses to FHB. This suggests that jasmonic acid may enhance wheat resistance to FHB by modulating the expression of TaG3LEA-25. Our results reveal a novel function of LEA gene, and TaG3LEA-25 could enrich the genebank for improving FHB resistance in wheat.
Keywords: TaG3LEA-25; Fusarium head blight; MYC2; Wheat protoplast-F. graminearum interaction; cytoskeleton; late embryogenesis abundant protein.
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