由 Ca2 信号调节的过敏反应程序性细胞死亡 (HR-PCD) 被认为是小麦抗小麦锈菌 (Pt.) 感染的主要调节因子。在这项研究中，面包小麦品种 Thatcher 及其带有叶锈病抗性基因座 Lr26 的近等基因系被 Pt 感染。 race 260 分别获得兼容和不兼容的组合。在感染 Pt. 后，通过不相容组合中的 Ca2 依赖性机制，翻译控制肿瘤蛋白 (TaTCTP) 的表达上调。 TaTCTP 的敲低显着增加了死亡细胞的面积和 Pt 的数量。感染部位的吸器母细胞（HMC），而过度表达该基因的植物表现出增强的抵抗力。还研究了 TaTCTP 和钙调神经磷酸酶 B 样蛋白相互作用蛋白激酶 23 (TaCIPK23) 之间的相互作用，发现这种相互作用发生在内质网中。 TaCIPK23 在体外磷酸化 TaTCTP。本塞姆氏烟草中磷酸模拟 TaTCTP 突变体的表达促进了 HR 样细胞死亡。沉默 TaCIPK23 或 TaCIPK23/TaTCTP 共沉默导致与沉默 TaTCTP 相同的结果。这表明TaTCTP是TaCIPK23的一个新的磷酸化靶标，两者均参与小麦对Pt的抗性。在同一路径中。© 2024 实验生物学协会和 John Wiley

Hypersensitive response-programmed cell death (HR-PCD) regulated by Ca2+ signal is considered the major regulator of resistance against Puccinia triticina (Pt.) infection in wheat. In this study, the bread wheat variety Thatcher and its near-isogenic line with the leaf rust resistance locus Lr26 were infected with the Pt. race 260 to obtain the compatible and incompatible combinations, respectively. The expression of translationally controlled tumor protein (TaTCTP) was upregulated upon infection with Pt., through a Ca2+-dependent mechanism in the incompatible combination. The knockdown of TaTCTP markedly increased the area of dying cell and the number of Pt. haustorial mother cells (HMCs) at the infection sites, whereas plants overexpressing the gene exhibited enhanced resistance. The interaction between TaTCTP and calcineurin B-like protein-interacting protein kinase 23 (TaCIPK23) was also investigated, and the interaction was found occurred in the endoplasmic reticulum. TaCIPK23 phosphorylated TaTCTP in vitro. The expression of a phospho-mimic TaTCTP mutant in Nicotiana benthamiana promoted HR-like cell death. Silencing TaCIPK23 or TaCIPK23/TaTCTP co-silencing resulted in the same results as silencing TaTCTP. This suggested that TaTCTP is a novel phosphorylation target of TaCIPK23, and both participate in the resistance of wheat to Pt. in the same pathway.© 2024 Society for Experimental Biology and John Wiley & Sons Ltd.