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MP西農(nóng)：鈣流在H2S調(diào)控ABA信號(hào)通路研究中充當(dāng)關(guān)鍵生理證據(jù)
2006~2020，NMT已扎根中國(guó)15年。2020年，中國(guó)NMT打開了歐洲市場(chǎng)，銷往瑞士蘇黎世大學(xué)，將開啟中歐合作新篇章。
相關(guān)閱讀：
1.【MP】西北農(nóng)林李積勝組*揭示硫化氫調(diào)控ABA信號(hào)通路的分子機(jī)制
2.Plant Cell 南農(nóng)：（H2O2流實(shí)驗(yàn)體系）硫化氫參與調(diào)節(jié)ABA誘導(dǎo)氣孔關(guān)閉的分子機(jī)制
3.Plant Cell | 南京農(nóng)業(yè)大學(xué)謝彥杰研究組揭示硫化氫參與調(diào)節(jié)ABA誘導(dǎo)氣孔關(guān)閉的分子機(jī)制
期刊：Molecular Plant
主題：硫化氫參與調(diào)節(jié)ABA調(diào)控氣孔關(guān)閉的分子機(jī)制
標(biāo)題：Hydrogen Sulfide Positively Regulates Abscisic Acid Signaling through Persulfidation of SnRK2.6 in Guard Cells
影響因子：10.812
檢測(cè)指標(biāo)：Ca2+流速
檢測(cè)樣品：擬南芥保衛(wèi)細(xì)胞
Ca2+流實(shí)驗(yàn)處理方法：
5周齡擬南芥幼苗，10μM ABA/100μM NaHS瞬時(shí)處理
Ca2+流實(shí)驗(yàn)測(cè)試液成份：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：西北農(nóng)林科技大學(xué)李積勝
保衛(wèi)細(xì)胞檢測(cè)視頻（轉(zhuǎn)自旭月公司）
中文摘要（谷歌機(jī)翻）
植物激素脫落酸（ABA）在觸發(fā)氣孔關(guān)閉和促進(jìn)植物適應(yīng)干旱脅迫方面起著關(guān)鍵作用。硫化氫（H2S）是一種小的信號(hào)氣體分子，與ABA依賴的氣孔關(guān)閉有關(guān)。但是，H2S如何調(diào)節(jié)ABA信號(hào)在很大程度上尚不清楚。
在這里，我們顯示ABA誘導(dǎo)L-半胱氨酸脫硫酶1（DES1）在保衛(wèi)細(xì)胞中催化H2S的產(chǎn)生，而H2S則通過開放氣孔1（OST1）/ SNF1相關(guān)蛋白激酶2.6（SnRK2）的過硫化而積極調(diào)節(jié)ABA信號(hào)傳導(dǎo)。.6）。暴露在SnRK2.6表面并靠近激活環(huán)的兩個(gè)半胱氨酸（Cys）位點(diǎn)Cys131和Cys137被鑒定為過硫化的，這促進(jìn)了SnRK2.6的活性及其與ABA反應(yīng)元件結(jié)合的相互作用factor2（ABF2），ABA信號(hào)下游的轉(zhuǎn)錄因子。
當(dāng)SnRK2.6中的Cys131，Cys137或兩者都被絲氨酸（S）取代時(shí)，H2S誘導(dǎo)的SnRK2.6活性和SnRK2.6-ABF2相互作用部分（SnRK2.6C131S和SnRK2.6C137S）或*（SnRK2.6C131SC137S）包括在內(nèi)。將snRK2.6C131S，SnRK2.6C137S或SnRK2.6C131SC137S引入ost1-3突變體無法挽救突變體表型，顯示出對(duì)ABA和H2S誘導(dǎo)的氣孔關(guān)閉和Ca2 +流入的敏感性較低，以及水分流失和干旱減少公差。
綜上所述，我們的研究揭示了一種新的ABA信號(hào)轉(zhuǎn)導(dǎo)后調(diào)控機(jī)制，其中H2S過硫化SnRK2.6以促進(jìn)ABA信號(hào)轉(zhuǎn)導(dǎo)和ABA誘導(dǎo)的氣孔關(guān)閉。
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 Sul?de (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.