5 years ago

Exogenous Hydrogen Peroxide Contributes to Heme Oxygenase-1 Delaying Programmed Cell Death in Isolated Aleurone Layers of Rice Subjected to Drought Stress in a cGMP-Dependent Manner.

Xiaojiang Deng, Huiping Chen, Yu Xiao, Guanghui Wang, Heting Zhang, Tingge Li
Hydrogen peroxide (H2O2) 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 ofHO-1transcript expression and HO activity. However, exogenous H2O2contributed toward the increase inHO-1gene expression and activity of the enzyme under drought stress. Meanwhile, the HO-1 inducer hematin could mimic the effects of the H2O2scavengers ascorbic acid (AsA) and dimethylthiourea (DMTU) and the H2O2synthesis inhibitor diphenyleneiodonium (DPI) for scavenging or diminishing drought-induced endogenous H2O2. Conversely, the zinc protoporphyrin IX (ZnPPIX), an HO-1-specific inhibitor, reversed the effects of hematin. We further analyzed the endogenous H2O2levels andHO-1transcript expression levels of aleurone layers treated with AsA, DMTU, and DPI in the presence of exogenous H2O2under drought stress, respectively. The results showed that in aleurone layers subjected to drought stress, when the endogenous H2O2level was inhibited, the effect of exogenous H2O2on the induction of HO-1 was enhanced. Furthermore, exogenous H2O2-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 H2O2-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 H2O2(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 H2O2promoted cell death.

Publisher URL: http://doi.org/10.3389/fpls.2018.00084

DOI: 10.3389/fpls.2018.00084

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