Wheat gliadins and glutenins confer valuable end-use characteristics but include amino acid sequences (epitopes) that can elicit celiac disease (CeD) in genetically predisposed individuals. The onset of CeD in these individuals is affected by the amount and duration of the exposure to immunogenic epitopes. Therefore, a reduction of epitopes that result in high immune responses in the majority of CeD patients (immunodominant epitopes) can reduce the incidence of CeD at a population level. We identified deletions encompassing the α-gliadins at the three wheat genomes, designated hereafter as Δgli-A2 (PI 704906), Δgli-B2 (PI 704907), and Δgli-D2 (PI 704908). The Δgli-D2 deletion, which eliminates major immunodominant epitopes, significantly increases gluten strength, improves breadmaking quality, and has no negative effects on grain yield or grain protein content. By contrast, Δgli-A2 and Δgli-B2 showed limited effects on breadmaking quality. The stronger effect of the Δgli-D2 deletion on gluten strength is associated with the presence of α-gliadins with seven cysteines in GLI-D2 that are absent in GLI-A2 and GLI-B2 loci, which all have α-gliadins with six cysteines. We show that α-gliadins with seven cysteines are incorporated into the gluten polymer, where they likely function as chain-terminators limiting the expansion of the gluten polymer and reducing its strength. In summary, the publicly available Δgli-D2 deletion developed in this study can be used to simultaneously improve wheat gluten strength and reduce immunodominant CeD epitopes.
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Rottersman et al. (2024) studied this question.
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