Hydrogen Sulfide Positively Regulates Abscisic Acid Signaling through Persulfidation of SnRK2.6 in Guard Cells
Hydrogen Sulfide Positively Regulates Abscisic Acid Signaling through Persulfidation of SnRK2.6 in Guard Cells
复制标题
硫化氢通过保卫细胞中 SnRK2.6 的过硫化作用积极调节脱落酸信号传导
DOI：
10.1016/j.molp.2020.01.004
复制
发表时间：
2020-05-04
期刊：
影响因子：
27.5
通讯作者：
Li, Jisheng
中科院分区：
文献类型：
--
作者：
Chen, Sisi;Jia, Honglei;Li, Jisheng
植物激素脱落酸（阿坝）在触发气孔关闭和促进植物适应干旱胁迫中起着关键作用。硫化氢（H2S）是一种信号小分子，参与ABA依赖的气孔关闭。然而，H2S如何调节阿坝信号转导仍不清楚。在这里，我们表明，阿坝诱导生产的H2S催化的L-半胱氨酸脱氢酶1（DES 1）在保卫细胞，和H2S反过来积极调节阿坝信号通过过硫化的开放气孔1（OST 1）/SNF 1相关蛋白激酶2.6（SnRK2.6）。SnRK2.6的两个半胱氨酸（Cys）位点Cys 131和Cys 137暴露在SnRK2.6的表面，靠近激活环，被鉴定为过硫化，这促进了SnRK2.6的活性及其与阿坝响应元件结合因子2（ABF 2）的相互作用，ABF 2是阿坝信号下游的转录因子。当SnRK2.6中的Cys 131、Cys 137或这两个残基被丝氨酸（S）取代时，H2S诱导的SnRK2.6活性和SnRK2.6-ABF 2相互作用部分（SnRK2.6（C）（131 S）和SnRK2.6（C）（137 S））或完全（SnRK2.6（C131 SC 137 S））受损。将SnRK2.6（C131 S）、SnRK2.6（C137 S）或SnRK2.6（C131 SC 137 S）导入ost 1 -3突变体不能挽救突变体表型：对阿坝和H2S诱导的气孔关闭和Ca 2+内流的敏感性降低以及水分损失增加和耐旱性降低。综上所述，我们的研究揭示了一种新的阿坝信号转导的翻译后调节机制，即H2S过硫化物SnRK2.6促进阿坝信号转导和ABA诱导的气孔关闭。
The phytohormone abscisic acid (ABA) plays pivotal roles in triggering stomatal closure and facilitating adaptation of plants to drought stress. Hydrogen sulfide (H2S), a small signaling gas molecule, is involved in ABA-dependent stomatal closure. However, how H2S regulates ABA signaling remains largely unclear. Here, we show that ABA induces the production of H2S catalyzed by L-CYSTEINE DESULFHYDRASE1 (DES1) in guard cells, and H2S in turn positively regulates ABA signaling through persulfidation of Open Stomata 1 (OST1)/SNF1-RELATED PROTEIN KINASE2.6 (SnRK2.6). Two cysteine (Cys) sites, Cys131 and Cys137, which are exposed on the surface of SnRK2.6 and close to the activation loop, were identified to be persulfidated, which promotes the activity of SnRK2.6 and its interaction with ABA response element-binding factor 2 (ABF2), a transcription factor acting downstream of ABA signaling. When Cys131, Cys137, or both residues in SnRK2.6 were substituted with serine (S), H2S-induced SnRK2.6 activity and SnRK2.6-ABF2 interaction were partially (SnRK2.6(C)(131S) and SnRK2.6(C)(137S)) or completely (SnRK2.6(C131SC137S)) compromised. Introduction of SnRK2.6(C131S) SnRK2.6(c137S), or SnRK2.6(C131SC137S) into the ost1-3 mutant could not rescue the mutant phenotype: less sensitivity to ABA- and H2S-induced stomatal closure and Ca2+ influx as well as increased water loss and decreased drought tolerance. Taken together, our study reveals a novel post-translational regulatory mechanism of ABA signaling whereby H2S persulfidates SnRK2.6 to promote ABA signaling and ABA-induced stomatal closure.