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 Malus hupehensis. MhSLAH3, a homolog of the slow anion channel from M. hupehensis, encoded a channel controlling Cl− efflux and was induced by both chloride and ABA. MhSLAH3 overexpression accelerated Cl− efflux, which enhanced the tolerance of M. hupehensis to chloride stress, and retarded chloride-induced cell death. However, the suppression of MhSLAH3 partially offset the acceleration effect of ABA on Cl− efflux. MhZAT10L was then identified as a C2H2-type transcription factor upstream of MhSLAH3, repressing MhSLAH3 transcription under chloride stress. The suppression of MhZAT10L accelerated Cl− efflux by releasing suppressed MhSLAH3, but MhZAT10L overexpression counteracted the effects of ABA on Cl− efflux. MhABI5 promoted Cl− efflux mediated by MhSLAH3 due to induction by ABA and transcriptional repression of MhZAT10L, but this function of MhABI5 was reversed by MhZAT10L overexpression. The suppression of MhABI5 diminished the positive effects of ABA on Cl− efflux and retarding cell death. Thus, ABA repressed MhZAT10L transcription by activating MhABI5, further releasing MhSLAH3 to accelerate Cl− efflux. These findings provide a new evidence of ABA regulation of Cl− efflux.

中文翻译：

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脱落酸通过 ABI5-ZAT10-SLAH3 模块调节氯化物胁迫的 Malus hupehensis 的 Cl− 外排


Cl− 的超载通常会导致植物细胞损伤和死亡，尤其是在对 Cl− 敏感的作物中。脱落酸 （ABA） 是一种应激诱导的植物激素，可以通过减少 Cl− 积累来缓解氯化物应激;然而，机制尚不清楚。在这里，我们发现 ABA 的应用提高了 Cl− 从根的外排，减少了氯化物胁迫的 Malus hupehensis 的膜损伤和细胞死亡。MhSLAH3 是湖北支原体慢阴离子通道的同源物，编码控制 Cl− 外排的通道，并被氯化物和 ABA 诱导。MhSLAH3 过表达加速了 Cl− 外排，从而增强了湖北分枝杆菌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，MhSLAH3 的抑制部分抵消了 ABA 对 Cl− 外排的加速作用。然后确定 MhZAT10L 是 MhSLAH3 上游的 C2H2 型转录因子，在氯化物胁迫下抑制 MhSLAH3 转录。MhZAT10L 的抑制通过释放抑制的 MhSLAH3 加速了 Cl− 外排，但 MhZAT10L 过表达抵消了 ABA 对 Cl− 外排的影响。由于 ABA 的诱导和 MhZAT10L 的转录抑制，MhABI5 促进了 MhSLAH3 介导的 Cl− 外排，但 MhABI5 的这一功能被 MhZAT10L 过表达逆转。MhABI5 的抑制降低了 ABA 对 Cl− 外排和延缓细胞死亡的积极影响。因此，ABA 通过激活 MhABI5 抑制 MhZAT10L 转录，进一步释放 MhSLAH3 以加速 Cl−外流。这些发现为 ABA 调节 Cl− 外排提供了新的证据。