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Abscisic acid-triggered guard cell l-cysteine desulfhydrase function and in situ hydrogen sulfide production contributes to heme oxygenase-modulated stomatal closure.
Plant, Cell & Environment ( IF 7.3 ) Pub Date : 2019-12-30 , DOI: 10.1111/pce.13685
Jing Zhang 1 , Mingjian Zhou 1 , Zhenglin Ge 1 , Jie Shen 1 , Can Zhou 1 , Cecilia Gotor 2 , Luis C Romero 2 , Xingliang Duan 1 , Xin Liu 3 , Deliang Wu 4, 5, 6 , Xianchao Yin 4, 5, 6 , Yanjie Xie 1
Affiliation  

Recent studies have demonstrated that hydrogen sulfide (H2 S) produced through the activity of l-cysteine desulfhydrase (DES1) is an important gaseous signaling molecule in plants that could participate in abscisic acid (ABA)-induced stomatal closure. However, the coupling of the DES1/H2 S signaling pathways to guard cell movement has not been thoroughly elucidated. The results presented here provide genetic evidence for a physiologically relevant signaling pathway that governs guard cell in situ DES1/H2 S function in stomatal closure. We discovered that ABA-activated DES1 produces H2 S in guard cells. The impaired guard cell ABA phenotype of the des1 mutant can be fully complemented when DES1/H2 S function has been specifically rescued in guard cells and epidermal cells, but not mesophyll cells. This research further characterized DES1/H2 S function in the regulation of LONG HYPOCOTYL1 (HY1, a member of the heme oxygenase family) signaling. ABA-induced DES1 expression and H2 S production are hyper-activated in the hy1 mutant, both of which can be fully abolished by the addition of H2 S scavenger. Impaired guard cell ABA phenotype of des1/hy1 can be restored by H2 S donors. Taken together, this research indicated that guard cell in situ DES1 function is involved in ABA-induced stomatal closure, which also acts as a pivotal hub in regulating HY1 signaling.

中文翻译:

脱落酸触发的保卫细胞L-半胱氨酸脱硫酶功能和原位硫化氢的产生有助于血红素加氧酶调节的气孔关闭。

最近的研究表明,通过l-半胱氨酸脱硫酶(DES1)的活性产生的硫化氢(H2 S)是植物中重要的气体信号分子,可以参与脱落酸(ABA)诱导的气孔关闭。但是,尚未彻底阐明DES1 / H2 S信号通路与保护细胞运动的耦合。此处提供的结果为控制气孔关闭中保卫细胞原位DES1 / H2 S功能的生理相关信号通路提供了遗传学证据。我们发现,ABA激活的DES1在保卫细胞中产生H2S。当在保卫细胞和表皮细胞而非叶肉细胞中特异性挽救了DES1 / H2 S功能后,des1突变体受损的保卫细胞ABA表型可以得到完全补充。这项研究进一步表征了DES1 / H2 S在调控长HYPOCOTYL1(HY1,血红素加氧酶家族的成员)信号传导中的功能。ABA诱导的DES1表达和H2 S的产生在hy1突变体中被过度激活,通过添加H2 S清除剂可以完全消除这两者。des1 / hy1的保卫细胞ABA表型受损可以被H2 S供体恢复。两者合计,这项研究表明,保卫细胞原位DES1功能与ABA诱导的气孔关闭有关,它也起着调节HY1信号转导的枢纽作用。des1 / hy1的保卫细胞ABA表型受损可以被H2 S供体恢复。两者合计,这项研究表明,保卫细胞原位DES1功能与ABA诱导的气孔关闭有关,它也起着调节HY1信号转导的枢纽作用。des1 / hy1的保卫细胞ABA表型受损可以被H2 S供体恢复。两者合计,这项研究表明,保卫细胞原位DES1功能与ABA诱导的气孔关闭有关,它也起着调节HY1信号转导的枢纽作用。
更新日期:2019-12-31
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