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MP西農：鈣流在H2S調控ABA信號通路研究中充當關鍵生理證據
2006~2020，NMT已扎根中國15年。2020年，中國NMT打開了歐洲市場，銷往瑞士蘇黎世大學，將開啟中歐合作新篇章。
相關閱讀：
1.【MP】西北農林李積勝組*揭示硫化氫調控ABA信號通路的分子機制
2.Plant Cell 南農：（H2O2流實驗體系）硫化氫參與調節ABA誘導氣孔關閉的分子機制
3.Plant Cell | 南京農業大學謝彥杰研究組揭示硫化氫參與調節ABA誘導氣孔關閉的分子機制
期刊：Molecular Plant
主題：硫化氫參與調節ABA調控氣孔關閉的分子機制
標題：Hydrogen Sulfide Positively Regulates Abscisic Acid Signaling through Persulfidation of SnRK2.6 in Guard Cells
影響因子：10.812
檢測指標：Ca2+流速
檢測樣品：擬南芥保衛細胞
Ca2+流實驗處理方法：
5周齡擬南芥幼苗，10μM ABA/100μM NaHS瞬時處理
Ca2+流實驗測試液成份：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：西北農林科技大學李積勝
保衛細胞檢測視頻（轉自旭月公司）
中文摘要（谷歌機翻）
植物激素脫落酸（ABA）在觸發氣孔關閉和促進植物適應干旱脅迫方面起著關鍵作用。硫化氫（H2S）是一種小的信號氣體分子，與ABA依賴的氣孔關閉有關。但是，H2S如何調節ABA信號在很大程度上尚不清楚。
在這里，我們顯示ABA誘導L-半胱氨酸脫硫酶1（DES1）在保衛細胞中催化H2S的產生，而H2S則通過開放氣孔1（OST1）/ SNF1相關蛋白激酶2.6（SnRK2）的過硫化而積極調節ABA信號傳導。.6）。暴露在SnRK2.6表面并靠近激活環的兩個半胱氨酸（Cys）位點Cys131和Cys137被鑒定為過硫化的，這促進了SnRK2.6的活性及其與ABA反應元件結合的相互作用factor2（ABF2），ABA信號下游的轉錄因子。
當SnRK2.6中的Cys131，Cys137或兩者都被絲氨酸（S）取代時，H2S誘導的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。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ABA和H2S誘導的氣孔關閉和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信號轉導后調控機制，其中H2S過硫化SnRK2.6以促進ABA信號轉導和ABA誘導的氣孔關閉。
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.