CRISPR-Cas9 genome editing systems have revolutionized plant gene functional studies by enabling the targeted introduction of insertion-deletions (INDELs) via the nonhomologous end-joining (NHEJ) pathway. Frameshift-inducing INDELs can introduce a premature termination codon and, in other instances, can lead to the appearance of new proteins. Here, we found that mutations in the rice jasmonate (JA) signaling gene OsJAZ10 by CRISPR-Cas9-based genome editing did not affect canonical JA signaling. However, a type of mutant with an INDEL that yielded a novel frameshift protein named FJ10 ( F rameshift mutation of J AZ 10 ), exhibited enhanced rice growth and increased resistance to brown planthopper attacks. Overexpression of FJ10 in wild-type plants phenocopies OsJAZ10 frameshift mutants. Further characterization revealed that FJ10 interacts with Slender Rice 1 (OsSLR1) and F-box/Kelch 16 (OsFBK16). These interactions disrupt the function of OsSLR1 in suppressing gibberellin-mediated growth and the function of OsFBK16 in repressing lignin-mediated defense responses, respectively. Field experiments with FJ10 -expressing plants demonstrate that this protein uncouples the growth–defense tradeoff, opening broad avenues to obtain cultivars with enhanced yield without compromised defenses.

中文翻译：

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JAZ10 中的移码突变解决了水稻生长与防御的困境


CRISPR-Cas9 基因组编辑系统通过非同源末端连接 （NHEJ） 通路靶向引入插入-缺失 （INDEL），彻底改变了植物基因功能研究。移码诱导的 INDEL 可以引入过早终止密码子，在其他情况下，会导致新蛋白质的出现。在这里，我们发现通过基于 CRISPR-Cas9 的基因组编辑对水稻茉莉酸酯 （JA） 信号基因 OsJAZ10 的突变不会影响经典 JA 信号传导。然而，一种具有 INDEL 的突变体产生一种名为 FJ10 的新型移码蛋白（J AZ 10 的 F 分枝突变），表现出增强的水稻生长和对褐飞虱攻击的抵抗力增加。在野生型植物表型拷贝 OsJAZ10 移码突变体中过表达 FJ10。进一步的表征显示，FJ10 与 Slender Rice 1 （OsSLR1） 和 F-box/Kelch 16 （OsFBK16） 相互作用。这些相互作用分别破坏了 OsSLR1 在抑制赤霉素介导的生长中的功能和 OsFBK16 在抑制木质素介导的防御反应中的功能。用表达 FJ10 的植物进行的田间实验表明，这种蛋白质解耦了生长-防御权衡，为获得产量更高的品种开辟了广阔的途径，而不会影响防御。