Journal of Advanced Research ( IF 11.4 ) Pub Date : 2020-07-25 , DOI: 10.1016/j.jare.2020.07.013 Jing Zhang 1 , Heng Zhou 1 , Mingjian Zhou 1 , Zhenglin Ge 1 , Feng Zhang 1 , Christine H Foyer 2 , Xingxing Yuan 3 , Yanjie Xie 1
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Introduction
Drought stress triggers the synthesis and accumulation of the phytohormone abscisic acid (ABA), which regulates stomatal aperture and hence reducing plant water loss. Hydrogen sulfide (H2S), which is produced by the enzyme L-cysteine desulfhydrase 1 (DES1) that catalyzes the desulfuration of L-cysteine in Arabidopsis, also plays a critical role in the regulation of drought-induced stomatal closure. However, little is known about the regulation of DES1 or the crosstalk between H2S and ABA signaling in response to dehydration.
Objectives
To demonstrate the potential crosstalk between DES1-dependent H2S and ABA signaling in response to dehydration and its regulation mechanism.
Methods
Firstly, by introducing guard cell-specific MYB60 promoter, to produce complementary lines of DES1 or ABA3 into guard cell of des1 or aba3 mutant. And the related genes expression and water loss under ABA, NaHS, or dehydration treatment in these mutant or transgenics lines were determinate.
Results
We found that dehydration-induced expression of DES1 is abolished in the abscisic acid deficient 3 (aba3) mutants that are deficient in ABA synthesis. Both the complementation of ABA3 expression in guard cells of the aba3 mutants and ABA treatment rescue the dehydration-induced expression of DES1, as well as the wilting phenotype observed in these mutants. Moreover, the drought-induced expression of ABA synthesis genes was suppressed in des1 mutants. While the addition of ABA or the expression of either ABA3 or DES1 in the guard cells of the aba3/des1 double mutant did not alter the wilting phenotype of these mutants, the wild type phenotype was fully restored by the expression of both ABA3 and DES1, or by the application of NaHS.
Conclusion
These results demonstrate that the coordinated synthesis of ABA and DES1 expression is required for drought-induced stomatal closure in Arabidopsis.
中文翻译：
保卫细胞自主ABA合成与原位DES1功能的协调调节植物缺水反应
介绍
干旱胁迫会触发植物激素脱落酸 (ABA) 的合成和积累，从而调节气孔孔径，从而减少植物水分流失。硫化氢 (H 2 S) 由催化拟南芥中 L-半胱氨酸脱硫的酶 L-半胱氨酸脱硫酶 1 (DES1) 产生，在调节干旱诱导的气孔关闭中也起着关键作用。然而，关于 DES1 的调节或 H 2 S 和 ABA 信号之间的串扰响应脱水知之甚少。
目标
证明 DES1 依赖性 H 2 S 和 ABA 信号之间的潜在串扰以响应脱水及其调节机制。
方法
首先，通过引入保卫细胞特异性MYB60启动子，在des1或aba3突变体的保卫细胞中产生DES1或ABA3的互补系。在ABA、NaHS或脱水处理下，这些突变或转基因品系的相关基因表达和失水量是确定的。
结果
我们发现脱水诱导的DES1表达在 ABA 合成缺陷的脱落酸缺陷 3 ( aba3 ) 突变体中被消除。aba3突变体保卫细胞中ABA3表达的互补和 ABA 处理都挽救了脱水诱导的DES1表达，以及在这些突变体中观察到的萎蔫表型。此外，干旱诱导的 ABA 合成基因的表达在des1突变体中受到抑制。而在aba3/des1的保卫细胞中添加 ABA 或ABA3或DES1的表达双突变体没有改变这些突变体的萎蔫表型，野生型表型通过ABA3和DES1的表达或NaHS的应用完全恢复。
结论
这些结果表明，ABA 和DES1表达的协同合成是拟南芥干旱诱导的气孔关闭所必需的。
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