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.

Full text PDF download