Drought stress induces stomatal closure and inhibits stomatal opening simultaneously. However, the underlying molecular mechanism is still largely unknown. Here we show that S-type anion channels SLAC1 and SLAH3 mainly inhibit inward K+ (K+in) channel KAT1 by protein-protein interaction, and consequently prevent stomatal opening in Arabidopsis. Voltage-clamp results demonstrated that SLAC1 inhibited KAT1 dramatically, but did not inhibit KAT2. SLAH3 inhibited KAT1 to a weaker degree relative to SLAC1. Both the N terminus and the C terminuses of SLAC1 inhibited KAT1, but the inhibition by the N terminus was stronger. The C terminus was essential for the inhibition of KAT1 by SLAC1. Furthermore, drought stress strongly up-regulated the expression of SLAC1 and SLAH3 in Arabidopsis guard cells, and the over-expression of wild type and truncated SLAC1 dramatically impaired K+in currents of guard cells and light-induced stomatal opening. Additionally, the inhibition of KAT1 by SLAC1 and KC1 only partially overlapped, suggesting that SLAC1 and KC1 inhibited K+in channels using different molecular mechanisms. Taken together, we discovered a novel regulatory mechanism for stomatal movement, in which singling pathways for stomatal closure and opening are directly coupled together by protein-protein interaction between SLAC1/SLAH3 and KAT1 in Arabidopsis.

干旱胁迫诱导气孔关闭并同时抑制气孔打开。但是，基本的分子机制仍是未知的。在这里，我们显示S型阴离子通道SLAC1和SLAH3主要通过蛋白-蛋白相互作用抑制内向K +（K + in）通道KAT1，从而防止拟南芥中的气孔开放。电压钳位结果表明SLAC1显着抑制KAT1，但不抑制KAT2。相对于SLAC1，SLAH3对KAT1的抑制程度较弱。SLAC1的N端和C端均抑制KAT1，但N端的抑制作用更强。C末端对于SLAC1抑制KAT1至关重要。此外，干旱胁迫强烈上调拟南芥保卫细胞中SLAC1和SLAH3的表达，并且野生型和截短的SLAC1的过表达极大地损害了保卫细胞和光诱导的气孔开放中的K +电流。此外，SLAC1和KC1对KAT1的抑制作用仅部分重叠，这表明SLAC1和KC1使用不同的分子机制抑制了K + in通道。综上所述，我们发现了一种新颖的气孔运动调节机制，其中通过拟南芥中SLAC1 / SLAH3和KAT1之间的蛋白-蛋白相互作用将气孔关闭和打开的单一途径直接耦合在一起。