摘要
Hydrogen sulfide （H2S） is a newly discovered gaseous signaling molecule and involved in ethylene and ABA-induced stomatal closure. As an important factor, extracellular ATP （eATP） was believed to participate in regulation of stomatal closing. However, the mechanism by which eATP mediates HES-regulated stomatal closure remains unclear. Here, we employed Arabidopsis wild-type and mutant lines of ATP-binding cassette transporters （Atmrp4, Atmrp5 and their double mutant Atmrp4/5） to study the function of eATP in H_2S-regulated stomatal movement. Our results indicated that H_2S affected stomatal closing through stimulating guard cell outward K^＋ current. Moreover, we found that HES induced eATP generation by regulating the activity of an ABC transporter. The inhibitor of ABC transporters, glibenclamide （Gli）, could impair H_2S-regulated stomatal closure and reduce H_2S-dependent eATP accumulation in Atmrp4 and Atmrp5 mutants. In addition, the promotion effect of H_2S on outward K^＋ currents was diminished in Atmrp4/5 double mutant. Our data suggested that hydrogen peroxide （H_2O_2） is required for H_2S-induced stomatal closure, and the production of H_2O_2 is regulated by eATP via NADPH oxidase. Based on this work, we conclude that H_2S-induced stomatal closure requires ABC transporter-dependent eATP pro- duction and subsequent NADPH oxidase-dependent H_2O_2 accumulation.
硫化氢(H2S)和通过ABC转运体转运至胞外形成的胞外ATP(eA TP)均参与对气孔运动的调控,但尚不清楚eA TP在H2S诱导气孔关闭中的作用机制.本研究显示,ABC转运体抑制剂和质膜嘌呤受体抑制剂能够抑制H2S诱导的气孔关闭和所引起的保卫细胞中H2O2水平的升高;但H2S不能引起Atmrp4、Atmrp5以及Atmrp4/5中eA TP的积累和保卫细胞中H2O2水平的升高;H2S亦不能引起Atmrp4/5保卫细胞原生质体K+外流.据此推论:H2S可通过eA TP调控H2O2,进而调节气孔保卫细胞钾离子通道诱导气孔关闭.
基金
supported by the National Natural Science Foundation of China(31170237)
the National Key Laboratory Program of China Agricultural University(SKLPPBKF11001)
Shandong Taishan Scholar Program
