Cultivated sweet potato (Ipomoea batatas) is an important source of food for both humans and domesticated animals. Here, we show that the B-box (BBX) family transcription factor IbBBX24 regulates the jasmonic acid (JA) pathway in sweet potato. When IbBBX24 was overexpressed in sweet potato, JA accumulation increased, whereas silencing this gene decreased JA levels. RNA sequencing analysis revealed that IbBBX24 modulates the expression of genes involved in the JA pathway. IbBBX24 regulates JA responses by antagonizing the JA signaling repressor IbJAZ10, which relieves IbJAZ10’s repression of IbMYC2, a JA signaling activator. IbBBX24 binds to the IbJAZ10 promoter and activates its transcription, whereas it represses the transcription of IbMYC2. The interaction between IbBBX24 and IbJAZ10 interferes with IbJAZ10’s repression of IbMYC2, thereby promoting the transcriptional activity of IbMYC2. Overexpressing IbBBX24 significantly increased Fusarium wilt disease resistance, suggesting that JA responses play a crucial role in regulating Fusarium wilt resistance in sweet potato. Finally, overexpressing IbBBX24 led to increased yields in sweet potato. Together, our findings indicate that IbBBX24 plays a pivotal role in regulating JA biosynthesis and signaling and increasing Fusarium wilt resistance and yield in sweet potato, thus providing a candidate gene for developing elite crop varieties with enhanced pathogen resistance but without yield penalty.

栽培的甘薯（番薯）是人类和家畜的重要食物来源。在这里，我们显示B-box（BBX）家族转录因子IbBBX24调节甘薯中的茉莉酸（JA）途径。当在甘薯中过表达IbBBX24时，JA积累增加，而沉默该基因会降低JA水平。RNA测序分析表明，IbBBX24调节JA途径中涉及的基因的表达。IbBBX24通过拮抗JA信号传导阻遏物IbJAZ10来调节JA响应，从而减轻IbJAZ10对JA信号传导激活剂IbMYC2的抑制。IbBBX24与IbJAZ10启动子结合并激活其转录，而它抑制IbMYC2的转录。IbBBX24和IbJAZ10之间的相互作用会干扰IbJAZ10对IbMYC2的抑制，从而促进IbMYC2的转录活性。过表达的IbBBX24显着提高了枯萎病的抗病性，这表明JA反应在调节甘薯枯萎病的抗性中起着至关重要的作用。最后，过表达的IbBBX24导致甘薯产量增加。总之，我们的发现表明，IbBBX24在调节JA生物合成和信号传导以及增加甘薯的枯萎病抗性和产量中起关键作用，从而为开发具有增强的病原体抗性但没有产量损失的优良农作物品种提供了候选基因。