Song Jianfei, Yan Junhong, Sun Baozhen, Chen Bing, Zhu Xiaoyue, Wei Hongcai, Bao Zhilong, Ma Fangfang, Zhang Weiwei, Yang Hongqiang
College of Horticulture Science and Engineering, Shandong Agricultural University, Tai'an, 271018, Shandong, China.
Apple Technology Innovation Center of Shandong Province, Tai'an, 271018, Shandong, China.
Hortic Res. 2024 Jul 24;11(9):uhae200. doi: 10.1093/hr/uhae200. eCollection 2024 Sep.
The overload of Cl typically causes cell damage and death in plants, especially in Cl-sensitive crops. Abscisic acid (ABA) is a stress-induced phytohormone that can alleviate chloride stress by reducing Cl accumulation; however, the mechanism is not clear. Here, we found that the application of ABA elevated Cl efflux from roots and reduced membrane damage and cell death in chloride-stressed . , a homolog of the slow anion channel from , encoded a channel controlling Cl efflux and was induced by both chloride and ABA. overexpression accelerated Cl efflux, which enhanced the tolerance of to chloride stress, and retarded chloride-induced cell death. However, the suppression of partially offset the acceleration effect of ABA on Cl efflux. MhZAT10L was then identified as a C2H2-type transcription factor upstream of , repressing transcription under chloride stress. The suppression of accelerated Cl efflux by releasing suppressed , but overexpression counteracted the effects of ABA on Cl efflux. MhABI5 promoted Cl efflux mediated by due to induction by ABA and transcriptional repression of , but this function of MhABI5 was reversed by overexpression. The suppression of diminished the positive effects of ABA on Cl efflux and retarding cell death. Thus, ABA repressed transcription by activating MhABI5, further releasing to accelerate Cl efflux. These findings provide a new evidence of ABA regulation of Cl efflux.
氯离子过载通常会导致植物细胞损伤和死亡，尤其是在对氯离子敏感的作物中。脱落酸（ABA）是一种应激诱导的植物激素，它可以通过减少氯离子积累来缓解氯化物胁迫；然而，其机制尚不清楚。在这里，我们发现施用ABA可提高根部的氯离子外流，减少氯化物胁迫下的膜损伤和细胞死亡。来自[具体物种]的慢阴离子通道的同源物[具体基因名称]编码一个控制氯离子外流的通道，并且受氯化物和ABA诱导。[具体基因名称]过表达加速了氯离子外流，增强了[具体植物名称]对氯化物胁迫的耐受性，并延缓了氯化物诱导的细胞死亡。然而，[具体基因名称]的抑制部分抵消了ABA对氯离子外流的加速作用。然后，MhZAT10L被鉴定为[具体基因名称]上游的C2H2型转录因子，在氯化物胁迫下抑制[具体基因名称]转录。[具体基因名称]的抑制通过释放受抑制的[具体基因名称]来加速氯离子外流，但[具体基因名称]过表达抵消了ABA对氯离子外流的影响。由于ABA诱导和[具体基因名称]的转录抑制，MhABI5促进了由[具体基因名称]介导的氯离子外流，但[具体基因名称]过表达逆转了MhABI5的这一功能。[具体基因名称]的抑制减弱了ABA对氯离子外流的积极影响并延缓细胞死亡。因此，ABA通过激活MhABI5抑制[具体基因名称]转录，进一步释放[具体基因名称]以加速氯离子外流。这些发现为ABA对氯离子外流的调控提供了新的证据。
