Rottersman Maria G, Zhang Wenjun, Zhang Junli, Grigorean Gabriela, Burguener German, Carter Claudia, Vang Teng, Hegarty Joshua, Zhang Xiaoqin, Finnie Sean, Dubcovsky Jorge
Department of Plant Sciences, University of California, One Shields Avenue, Davis, CA, 95616, USA.
Proteomics Core Facility, University of California, 451 E. Health Sciences Dr., Davis, CA, 95616, USA.
Theor Appl Genet. 2025 Apr 8;138(5):94. doi: 10.1007/s00122-025-04882-3.
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) may reduce the incidence of CeD at a population level. We generated gamma radiation-induced deletions encompassing the α-gliadins in each of the three wheat genomes and characterized them using exome capture. These deletions, designated as Δgli-A2, Δgli-B2, and Δgli-D2, were deposited in GRIN-Global. The Δgli-A2 and Δgli-B2 deletions showed limited effects on breadmaking quality, but the Δgli-D2 deletion significantly increased gluten strength and improved breadmaking quality without compromising dough elasticity, protein content, or grain yield. The stronger effect of Δgli-D2 on gluten strength was associated with an increased proportion of glutenins and the deletion of α-gliadins with seven cysteines, which are absent in the GLI-A2 and GLI-B2 loci. 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 addition to its beneficial effects on breadmaking quality, the Δgli-D2 deletion eliminates major wheat immunodominant CeD epitopes. The deployment of this publicly available Δgli-D2 deletion can simultaneously improve wheat gluten strength and reduce the population-wide burden of CeD.
小麦醇溶蛋白和谷蛋白赋予了有价值的最终使用特性,但包含的氨基酸序列(表位)可在遗传易感个体中引发乳糜泻(CeD)。这些个体中CeD的发病受免疫原性表位暴露量和持续时间的影响。因此,减少在大多数CeD患者中引发高免疫反应的表位(免疫显性表位)可能会在人群水平上降低CeD的发病率。我们通过γ射线诱导产生了涵盖三个小麦基因组中每个基因组的α-醇溶蛋白的缺失,并使用外显子捕获对其进行了表征。这些缺失被命名为Δgli-A2、Δgli-B2和Δgli-D2,并已存入GRIN-Global。Δgli-A2和Δgli-B2缺失对面包制作品质的影响有限,但Δgli-D2缺失显著提高了面筋强度并改善了面包制作品质,同时不影响面团弹性、蛋白质含量或谷物产量。Δgli-D2对面筋强度的更强影响与谷蛋白比例增加以及七个半胱氨酸的α-醇溶蛋白缺失有关,而这些在GLI-A2和GLI-B2基因座中不存在。我们表明,含有七个半胱氨酸的α-醇溶蛋白被整合到面筋聚合物中,它们可能在其中起到链终止剂的作用,限制面筋聚合物的扩展并降低其强度。除了对面包制作品质有有益影响外,Δgli-D2缺失还消除了主要的小麦免疫显性CeD表位。这种公开可用的Δgli-D2缺失的应用可以同时提高小麦面筋强度并减轻CeD在人群中的负担。