Wu Nan, Jiang Wanqing, Xiang Zhaoxia, Asghar Raheel, Akkaya Mahinur S
School of Bioengineering, Dalian University of Technology, No. 2 Linggong Road, Dalian 116024, China.
National Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Hubei Key Laboratory of Plant Pathology, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.
Plants (Basel). 2025 Jan 19;14(2):278. doi: 10.3390/plants14020278.
Plant immunity is largely governed by nucleotide-binding leucine-rich repeat receptor (NLR). Here, we examine the molecular activation and inhibition mechanisms of the wheat CC-type NLR , a previously proposed candidate for the resistance gene. Though recent studies have identified as the true gene, Yr10 remains an important NLR in understanding NLR-mediated immunity in wheat. In this study, we found that the overexpression of either the full-length Yr10 or its CC domain in did not trigger cell death, suggesting a robust autoinhibitory mechanism within Yr10. However, we observed that mutations in the conserved MHD motif, specifically D502G, activated Yr10 and induced cell death. Structural modeling indicated that this mutation disrupted key interactions within the MHD motif, promoting local flexibility and activation. We further explored the effector recognition potential of Yr10 by creating chimeric proteins with Sr50 domains, revealing that both the NB-ARC and LRR domains are necessary for effector recognition, while the CC domain likely functions in downstream immune signaling. Additionally, disrupting membrane localization through an L11E mutation abolished Yr10 self-activation, suggesting a requirement for membrane association in immune activation. Our findings contribute to the understanding of CC-NLR activation and autoinhibition mechanisms, highlighting the potential of Yr10 in NLR engineering for crop resistance improvement.
植物免疫很大程度上由核苷酸结合富含亮氨酸重复序列受体（NLR）控制。在此，我们研究了小麦CC型NLR的分子激活和抑制机制，该NLR是先前提出的一个抗病基因候选者。尽管最近的研究已确定Yr10为真正的抗病基因，但在理解小麦中NLR介导的免疫方面，Yr10仍然是一个重要的NLR。在本研究中，我们发现全长Yr10或其CC结构域在酵母中过表达均未引发细胞死亡，这表明Yr10内部存在强大的自抑制机制。然而，我们观察到保守的MHD基序中的突变，特别是D502G，激活了Yr10并诱导细胞死亡。结构建模表明，该突变破坏了MHD基序内的关键相互作用，促进了局部灵活性和激活。我们通过构建具有Sr50结构域的嵌合蛋白进一步探索了Yr10的效应子识别潜力，结果表明NB-ARC和LRR结构域对于效应子识别都是必需的，而CC结构域可能在下游免疫信号传导中起作用。此外，通过L11E突变破坏膜定位消除了Yr10的自激活，这表明免疫激活需要膜结合。我们的研究结果有助于理解CC-NLR的激活和自抑制机制，突出了Yr10在NLR工程中用于改善作物抗性的潜力。
