Zhengzhou Research Base, National Key Laboratory of Cotton Bio-breeding and Integrated Utilization, Zhengzhou University, Zhengzhou, 450000, China.
National Key Laboratory of Cotton Bio-breeding and Integrated Utilization, Institute of Cotton Research, Chinese Academy of Agricultural Sciences, Anyang, 455000, China.
Genome Biol. 2023 May 10;24(1):111. doi: 10.1186/s13059-023-02950-9.
Verticillium wilt is one of the most devasting diseases for many plants, leading to global economic loss. Cotton is known to be vulnerable to its fungal pathogen, Verticillium dahliae, yet the related genetic mechanism remains unknown.
By genome-wide association studies of 419 accessions of the upland cotton, Gossypium hirsutum, we identify ten loci that are associated with resistance against Verticillium wilt. Among these loci, SHZDI1/SHZDP2/AYDP1 from chromosome A10 is located on a fragment introgressed from Gossypium arboreum. We characterize a large cluster of Toll/interleukin 1 (TIR) nucleotide-binding leucine-rich repeat receptors in this fragment. We then identify a dual-TIR domain gene from this cluster, GhRVD1, which triggers an effector-independent cell death and is induced by Verticillium dahliae. We confirm that GhRVD1 is one of the causal gene for SHZDI1. Allelic variation in the TIR domain attenuates GhRVD1-mediated resistance against Verticillium dahliae. Homodimerization between TIR1-TIR2 mediates rapid immune response, while disruption of its αD- and αE-helices interface eliminates the autoactivity and self-association of TIR1-TIR2. We further demonstrate that GhTIRP1 inhibits the autoactivity and self-association of TIR1-TIR2 by competing for binding to them, thereby preventing the resistance to Verticillium dahliae.
We propose the first working model for TIRP1 involved self-association and autoactivity of dual-TIR domain proteins that confer compromised pathogen resistance of dual-TIR domain proteins in plants. The findings reveal a novel mechanism on Verticillium dahliae resistance and provide genetic basis for breeding in future.
黄萎病是许多植物最具破坏性的疾病之一，导致全球经济损失。棉花已知易受其真菌病原体黄萎病菌的影响，但相关的遗传机制尚不清楚。
通过对 419 份陆地棉（Gossypium hirsutum）品系的全基因组关联研究，我们鉴定出 10 个与抗黄萎病相关的位点。在这些位点中，来自染色体 A10 的 SHZDI1/SHZDP2/AYDP1 位于从 Gossypium arboreum 导入的片段上。我们在这个片段中鉴定出一个 Toll/白细胞介素 1（TIR）核苷酸结合富含亮氨酸重复受体的大簇。然后，我们从这个簇中鉴定出一个双 TIR 结构域基因 GhRVD1，它触发了一种不依赖效应物的细胞死亡，并被黄萎病菌诱导。我们证实 GhRVD1 是 SHZDI1 的一个候选基因。TIR 结构域的等位变异减弱了 GhRVD1 对黄萎病菌的抗性。TIR1-TIR2 之间的同源二聚化介导快速免疫反应，而破坏其αD-和αE-螺旋界面消除了 TIR1-TIR2 的自动活性和自聚集。我们进一步证明 GhTIRP1 通过竞争结合来抑制 TIR1-TIR2 的自动活性和自聚集，从而防止对黄萎病菌的抗性。
我们提出了第一个涉及双 TIR 结构域蛋白自聚集和自动活性的 TIRP1 工作模型，该模型导致植物中双 TIR 结构域蛋白对病原体抗性的降低。这些发现揭示了黄萎病菌抗性的一个新机制，并为未来的育种提供了遗传基础。
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