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MP西农:钙流在H2S调控ABA信号通路研究中充当关键生理证据

转自中关村旭月非损伤微测技术产业联盟


期刊:Molecular Plant
主题:硫化氢参与调节ABA调控气孔关闭的分子机制
标题:Hydrogen Sulfide Positively Regulates Abscisic Acid Signaling through Persulfidation of SnRK2.6 in Guard Cells
影响因子:10.812
检测指标:Ca2+流速
检测样品:拟南芥保卫细胞
Ca2+流实验处理方法:5周龄拟南芥幼苗,10μM ABA/100μM NaHS瞬时处理
Ca2+流实验测试液成份:Ca2+:0.1 mM KCl, 0.1 mM CaCl2, 0.1 mM MgCl2, 0.5 mM NaCl, 0.3 mM MES, 0.2 mM Na2SO4, pH 6.0
作者:西北农林科技大学李积胜

保卫细胞检测(转自旭月公司)

英文摘要

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 that are exposed on the surface of SnRK2.6 and closed to the activation loop, were identified to be persulfidated, which promotes the activity of SnRK2.6 and its interaction with ABA response element-binding factor2 (ABF2), a transcription factor downstream of ABA signaling.

When Cys131, Cys137 or both in SnRK2.6 was substituted with Serine (S), H2S-induced SnRK2.6 activity and SnRK2.6-ABF2 interaction were partially (SnRK2.6C131S and SnRK2.6C137S) or completely (SnRK2.6C131SC137S) comprised. Introduction of SnRK2.6C131S, SnRK2.6C137S, or SnRK2.6C131SC137S into ost1-3 mutant could not rescue the mutant phenotype, showing less sensitive 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 in which H2S persulfidates SnRK2.6 to promote ABA signaling and ABA-induced stomatal closure.

中文摘要(谷歌机翻)

植物激素脱落酸(ABA)在触发气孔关闭和促进植物适应干旱胁迫方面起着关键作用。硫化氢(H2S)是一种小的信号气体分子,与ABA依赖的气孔关闭有关。但是,H2S如何调节ABA信号在很大程度上尚不清楚。

在这里,我们显示ABA诱导L-半胱氨酸脱硫酶1(DES1)在保卫细胞中催化H2S的产生,而H2S则通过开放气孔1(OST1)/ SNF1相关蛋白激酶2.6(SnRK2)的过硫化而积极调节ABA信号传导。.6)。暴露在SnRK2.6表面并靠近激活环的两个半胱氨酸(Cys)位点Cys131和Cys137被鉴定为过硫化的,这促进了SnRK2.6的活性及其与ABA反应元件结合的相互作用factor2(ABF2),ABA信号下游的转录因子。

当SnRK2.6中的Cys131,Cys137或两者都被丝氨酸(S)取代时,H2S诱导的SnRK2.6活性和SnRK2.6-ABF2相互作用部分(SnRK2.6C131S和SnRK2.6C137S)或完全(SnRK2.6C131SC137S)包括在内。将snRK2.6C131S,SnRK2.6C137S或SnRK2.6C131SC137S引入ost1-3突变体无法挽救突变体表型,显示出对ABA和H2S诱导的气孔关闭和Ca2 +流入的敏感性较低,以及水分流失和干旱减少公差。

综上所述,我们的研究揭示了一种新的ABA信号转导后调控机制,其中H2S过硫化SnRK2.6以促进ABA信号转导和ABA诱导的气孔关闭。

文章链接:https://www.sciencedirect.com/science/article/pii/S1674205220300046?via%3Dihub

 

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