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Precise genome editing of Dense and Erect Panicle 1 promotes rice sheath blight resistance and yield production in japonica rice
Wednesday, 2025/03/19 | 08:23:30

Hongyao ZhuTiange ZhouJiaming GuanZhuo LiXiurong YangYuejiao LiJian SunQuan XuYuan Hu Xuan

Plant Biotechnology Journal; 4 March 2025; https://doi.org/10.1111/pbi.70010

Summary

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.

 

See https://onlinelibrary.wiley.com/doi/full/10.1111/pbi.70010

 

Figure 6:

dep1-cys enhanced the interaction with IDD10, resulting in decreased expression of ETR2. Y2H experiment (a) and CoIP assay (c, d) revealed that the interaction between IDD10 and DEP1 was weaker than that between IDD10 and dep1-cys. 3-amino-1,2,4-triazole (3-AT), a competitive inhibitor of HIS2, was used to suppress the self-activation of BD vectors. BiFC techniques (b) and LCA (e, f) demonstrated that the interaction between IDD10 and dep1-cys is stronger than that between IDD10 and DEP1. The numbers 1–4 in (d, e) are used to represent the interaction between IDD10 and dep1-cys, IDD10 and DEP1, BIK1 and RbohD as well as IDD10 and CIPK31, respectively. (g) The expression levels of ETR2 in WT, dep1, and dep1-cys were determined by RT-qPCR. Data are presented as the mean ± standard error (SE) of three replicates. Y1H (h) and Luciferase assay (i–k) indicated that both DEP1 and dep1-cys inhibit the DNA-binding ability of IDD10, and the inhibitory degree of dep1-cys was more prominent. The effects of AVG treatment on WT and dep1-cys resistance to ShB were photographed (l) and calculated (m). Data are presented as the mean ± standard deviation (n > 3). Different lowercase letters indicate significant differences at P < 0.05.

 

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