Wang Guanghui, Xiao Yu, Deng Xiaojiang, Zhang Heting, Li Tingge, Chen Huiping
Hainan Key Laboratory for Sustainable Utilization of Tropical Bioresource, Hainan University, Haikou, China.
Institute of Tropical Agriculture and Forestry, Hainan University, Haikou, China.
Front Plant Sci. 2018 Feb 1;9:84. doi: 10.3389/fpls.2018.00084. eCollection 2018.
Hydrogen peroxide (HO) is a reactive oxygen species (ROS) that plays a dual role in plant cells. Here, we discovered that drought (20% polyethylene glycol-6000, PEG)-triggered decreases of transcript expression and HO activity. However, exogenous HO contributed toward the increase in gene expression and activity of the enzyme under drought stress. Meanwhile, the HO-1 inducer hematin could mimic the effects of the HO scavengers ascorbic acid (AsA) and dimethylthiourea (DMTU) and the HO synthesis inhibitor diphenyleneiodonium (DPI) for scavenging or diminishing drought-induced endogenous HO. Conversely, the zinc protoporphyrin IX (ZnPPIX), an HO-1-specific inhibitor, reversed the effects of hematin. We further analyzed the endogenous HO levels and transcript expression levels of aleurone layers treated with AsA, DMTU, and DPI in the presence of exogenous HO under drought stress, respectively. The results showed that in aleurone layers subjected to drought stress, when the endogenous HO level was inhibited, the effect of exogenous HO on the induction of HO-1 was enhanced. Furthermore, exogenous HO-activated HO-1 effectively enhanced amylase activity. Application of 8-bromoguanosine 3',5'-cyclic guanosine monophosphate (8-Br-cGMP) (the membrane permeable cGMP analog) promoted the effect of exogenous HO-delayed PCD of aleurone layers in response to drought stress. More importantly, HO-1 delayed the programmed cell death (PCD) of aleurone layers by cooperating with nitric oxide (NO), and the delayed effect of NO on PCD was achieved via mediation by cGMP under drought stress. In short, in rice aleurone layers, exogenous HO (as a signaling molecule) triggered HO-1 and delayed PCD via cGMP which possibly induced amylase activity under drought stress. In contrast, as a toxic by-product of cellular metabolism, the drought-generated HO promoted cell death.
过氧化氢（HO）是一种活性氧（ROS），在植物细胞中发挥着双重作用。在此，我们发现干旱（20%聚乙二醇-6000，PEG）引发转录本表达和HO活性降低。然而，外源HO有助于在干旱胁迫下增加基因表达和该酶的活性。同时，HO-1诱导剂血晶素可模拟HO清除剂抗坏血酸（AsA）和二甲基硫脲（DMTU）以及HO合成抑制剂二苯基碘鎓（DPI）清除或减少干旱诱导的内源性HO的作用。相反，HO-1特异性抑制剂锌原卟啉IX（ZnPPIX）可逆转血晶素的作用。我们进一步分别分析了在干旱胁迫下外源HO存在时用AsA、DMTU和DPI处理的糊粉层的内源性HO水平和转录本表达水平。结果表明，在遭受干旱胁迫的糊粉层中，当内源性HO水平受到抑制时，外源HO对HO-1的诱导作用增强。此外，外源HO激活的HO-1有效增强了淀粉酶活性。应用8-溴鸟苷3',5'-环磷酸鸟苷（8-Br-cGMP）（膜通透性cGMP类似物）促进了外源HO延迟糊粉层响应干旱胁迫的程序性细胞死亡（PCD）的作用。更重要的是，HO-1通过与一氧化氮（NO）协同作用延迟了糊粉层的程序性细胞死亡（PCD），并且在干旱胁迫下，NO对PCD的延迟作用是通过cGMP介导实现的。简而言之，在水稻糊粉层中，外源HO（作为一种信号分子）通过cGMP触发HO-1并延迟PCD，这可能在干旱胁迫下诱导淀粉酶活性。相比之下，作为细胞代谢的有毒副产物，干旱产生的HO促进细胞死亡。
