College of Horticulture, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Key Laboratory of Protected Horticultural Engineering in Northwest, Ministry of Agriculture, Yangling, Shaanxi, 712100, China.
Plant J. 2024 Jun;118(6):1774-1792. doi: 10.1111/tpj.16709. Epub 2024 Mar 11.
Saline-alkali stress is an important abiotic stress factor affecting tomato (Solanum lycopersicum L.) plant growth. Although the involvement of the tomato SlWRKY gene family in responses to saline-alkali stress has been well established, the mechanism underlying resistance to saline-alkali stress remains unclear. In this study, we investigated the role of SlWRKY81 in conferring saline-alkali stress resistance by using overexpression and knockout tomato seedlings obtained via genetic modification. We demonstrated that SlWRKY81 improves the ability of tomato to withstand saline-alkali stress by enhancing antioxidant capacity, root activity, and proline content while reducing malondialdehyde levels. Saline-alkali stress induces an increase in jasmonic acid (JA) content in tomato seedlings, and the SlWRKY81 promoter responds to JA signaling, leading to an increase in SlWRKY81 expression. Furthermore, the interaction between SlJAZ1 and SlWRKY81 represses the expression of SlWRKY81. SlWRKY81 binds to W-box motifs in the promoter regions of SlSPDS2 and SlNHX4, thereby positively regulating their expression. This regulation results in increased spermidine (Spd) content and enhanced potassium (K) absorption and sodium (Na) efflux, which contribute to the resistance of tomato to saline-alkali stress. However, JA and SlJAZ1 exhibit antagonistic effects. Elevated JA content reduces the inhibitory effect of SlJAZ1 on SlWRKY81, leading to the release of additional SlWRKY81 protein and further augmenting the resistance of tomato to saline-alkali stress. In summary, the modulation of Spd synthesis and Na/K homeostasis mediated by the interaction between SlWRKY81 and SlJAZ1 represents a novel pathway underlying tomato response to saline-alkali stress.
盐碱性胁迫是影响番茄（Solanum lycopersicum L.）植株生长的重要非生物胁迫因素。尽管番茄 SlWRKY 基因家族参与盐碱性胁迫响应的机制已经得到很好的证实，但对其耐盐碱性的机制仍不清楚。在本研究中，我们通过遗传修饰获得的过表达和敲除番茄幼苗，研究了 SlWRKY81 在赋予番茄耐盐碱性方面的作用。研究结果表明，SlWRKY81 通过增强抗氧化能力、根活力和脯氨酸含量，同时降低丙二醛水平，提高番茄耐盐碱性。盐碱性胁迫诱导番茄幼苗中茉莉酸（JA）含量增加，SlWRKY81 启动子对 JA 信号作出响应，导致 SlWRKY81 表达增加。此外，SlJAZ1 和 SlWRKY81 之间的相互作用抑制 SlWRKY81 的表达。SlWRKY81 结合 SlSPDS2 和 SlNHX4 启动子区域中的 W-box 基序，从而正向调控其表达。这种调控导致亚精胺（Spd）含量增加，钾（K）吸收和钠（Na）外排增强，从而增强番茄对盐碱性胁迫的抗性。然而，JA 和 SlJAZ1 表现出拮抗作用。JA 含量的增加降低了 SlJAZ1 对 SlWRKY81 的抑制作用，释放出更多的 SlWRKY81 蛋白，进一步增强了番茄对盐碱性胁迫的抗性。综上所述，SlWRKY81 和 SlJAZ1 之间的相互作用介导的 Spd 合成和 Na/K 平衡的调节代表了番茄响应盐碱性胁迫的新途径。
