Yang Jie, Qiu Lina, Mei Quanlin, Sun Yunxia, Li Na, Gong Xiaoqing, Ma Fengwang, Mao Ke
State Key Laboratory of Crop Stress Biology for Arid Areas/Shaanxi Key Laboratory of Apple, College of Horticulture, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Plant J. 2023 Nov;116(3):669-689. doi: 10.1111/tpj.16395. Epub 2023 Jul 20.
Salt stress adversely affects the yield and quality of crops and limits their geographical distribution. Studying the functions and regulatory mechanisms of key genes in the salt stress response is important for breeding crops with enhanced stress resistance. Autophagy plays an important role in modulating the tolerance of plants to various types of abiotic stressors. However, the mechanisms underlying salt-induced autophagy are largely unknown. Cation/Ca exchanger proteins enhance apple salt tolerance by inhibiting Na accumulation but the mechanism underlying the response to salt stress remains unclear. Here, we show that the autophagy-related gene MdATG18a modulated apple salt tolerance. Under salt stress, the autophagic activity, proline content, and antioxidant enzyme activities were higher and Na accumulation was lower in MdATG18a-overexpressing transgenic plants than in control plants. The use of an autophagy inhibitor during the salt treatment demonstrated that the regulatory function of MdATG18a depended on autophagy. The yeast-one-hybrid assay revealed that the homeodomain-leucine zipper (HD-Zip) transcription factor MdHB7-like directly bound to the MdATG18a promoter. Transcriptional regulation and genetic analyses showed that MdHB7-like enhanced salt-induced autophagic activity by promoting MdATG18a expression. The analysis of Na efflux rate in transgenic yeast indicated that MdCCX1 expression significantly promoted Na efflux. Promoter binding, transcriptional regulation, and genetic analyses showed that MdHB7-like promoted Na efflux and apple salt tolerance by directly promoting MdCCX1 expression, which was independent of the autophagy pathway. Overall, our findings provide insight into the mechanism underlying MdHB7-like-mediated salt tolerance in apple through the MdHB7-like-MdATG18a and MdHB7-like-MdCCX1 modules. These results will aid future studies on the mechanisms underlying stress-induced autophagy and the regulation of stress tolerance in plants.
盐胁迫对作物的产量和品质产生不利影响，并限制其地理分布。研究盐胁迫响应中关键基因的功能和调控机制对于培育抗逆性增强的作物具有重要意义。自噬在调节植物对各种非生物胁迫的耐受性方面发挥着重要作用。然而，盐诱导自噬的潜在机制在很大程度上尚不清楚。阳离子/钙交换蛋白通过抑制钠积累增强苹果的耐盐性，但对盐胁迫响应的潜在机制仍不清楚。在这里，我们表明自噬相关基因MdATG18a调节苹果的耐盐性。在盐胁迫下，MdATG18a过表达转基因植物的自噬活性、脯氨酸含量和抗氧化酶活性较高，钠积累量低于对照植物。在盐处理期间使用自噬抑制剂表明MdATG18a的调节功能依赖于自噬。酵母单杂交试验表明，同源域-亮氨酸拉链（HD-Zip）转录因子MdHB7-like直接与MdATG18a启动子结合。转录调控和遗传分析表明，MdHB7-like通过促进MdATG18a表达增强盐诱导的自噬活性。转基因酵母中钠外流率的分析表明，MdCCX1表达显著促进钠外流。启动子结合、转录调控和遗传分析表明，MdHB7-like通过直接促进MdCCX1表达促进钠外流和苹果耐盐性，这与自噬途径无关。总体而言，我们的研究结果揭示了通过MdHB7-like-MdATG18a和MdHB7-like-MdCCX1模块介导苹果耐盐性的潜在机制。这些结果将有助于未来对胁迫诱导自噬机制和植物胁迫耐受性调控的研究。
