Abscisic acid regulates Cl efflux via the ABI5-ZAT10-SLAH3 module in chloride-stressed .

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.