Zhu Hongyao, Zhou Tiange, Guan Jiaming, Li Zhuo, Yang Xiurong, Li Yuejiao, Sun Jian, Xu Quan, Xuan Yuan Hu
State Key Laboratory of Elemento-Organic Chemistry and Department of Plant Protection, National Pesticide Engineering Research Center (Tianjin), Nankai University, Tianjin, China.
College of Plant Protection, Shenyang Agricultural University, Shenyang, China.
Plant Biotechnol J. 2025 May;23(5):1832-1846. doi: 10.1111/pbi.70010. Epub 2025 Mar 4.
The primary goals of crop breeding are to enhance yield and improve disease resistance. However, the "trade-off" mechanism, in which signalling pathways for resistance and yield are antagonistically regulated, poses challenges for achieving both simultaneously. Previously, we demonstrated that knock-out mutants of the Dense and Erect Panicle 1 (DEP1) gene can significantly enhance rice resistance to sheath blight (ShB), and we mapped DEP1's association with panicle length. In this study, we discovered that dep1 mutants significantly reduced rice yield. Nonetheless, truncated DEP1 was able to achieve both ShB resistance and yield increase in japonica rice. To further explore the function of truncated DEP1 in promoting yield and ShB resistance, we generated CRISPR/Cas9-mediated genome editing mutants, including a full-length deletion mutant of DEP1, named dep1, and a truncated version, dep1-cys. Upon inoculation with Rhizoctonia solani, the dep1-cys mutant demonstrated stronger ShB resistance than the dep1 mutant. Additionally, dep1-cys increased yield per plant, whereas dep1 reduced it. Compared to the full DEP1 protein, the truncated DEP1 (dep1-cys) demonstrated a decreased interaction affinity with IDD14 and increased affinity with IDD10, which are known to positively and negatively regulate ShB resistance through the activation of PIN1a and ETR2, respectively. The dep1-cys mutant exhibited higher PIN1a and lower ETR2 expression than wild-type plants, suggesting that dep1-cys modulated IDD14 and IDD10 interactions to regulate PIN1a and ETR2, thereby enhancing ShB resistance. Overall, these data indicate that precise genome editing of DEP1 could simultaneously improve both ShB resistance and yield, effectively mitigating trade-off regulation in rice.
作物育种的主要目标是提高产量和增强抗病性。然而，抗性和产量的信号通路相互拮抗调节的“权衡”机制，给同时实现这两个目标带来了挑战。此前，我们证明了密穗直立穗1（DEP1）基因的敲除突变体可显著增强水稻对纹枯病（ShB）的抗性，并且我们定位了DEP1与穗长的关联。在本研究中，我们发现dep1突变体显著降低了水稻产量。尽管如此，截短的DEP1能够在粳稻中实现对纹枯病的抗性和产量的增加。为了进一步探究截短的DEP1在促进产量和纹枯病抗性方面的功能，我们生成了CRISPR/Cas9介导的基因组编辑突变体，包括DEP1的全长缺失突变体dep1和截短版本dep1-cys。接种立枯丝核菌后，dep1-cys突变体表现出比dep1突变体更强的纹枯病抗性。此外，dep1-cys增加了单株产量，而dep1则降低了单株产量。与全长DEP1蛋白相比，截短的DEP1（dep1-cys）与IDD14的相互作用亲和力降低，与IDD10的亲和力增加，已知IDD14和IDD10分别通过激活PIN1a和ETR2对纹枯病抗性起正向和负向调节作用。dep1-cys突变体比野生型植株表现出更高的PIN1a表达和更低的ETR2表达，表明dep1-cys调节了IDD14和IDD10的相互作用以调控PIN1a和ETR2，从而增强了纹枯病抗性。总体而言，这些数据表明对DEP1进行精确的基因组编辑可同时提高纹枯病抗性和产量，有效缓解水稻中的权衡调节。
