title: Reactive oxygen species-provoked mitochondria-dependent cell death during ageing of elm (Ulmus pumila L.) seeds.
abstract: Previous studies have shown that controlled deterioration treatment (CDT) induces programmed cell death in elm (Ulmus pumila L.) seeds, which undergo certain fundamental processes that are comparable to apoptosis in animals. In this study, the essential characteristics of mitochondrial physiology in elm seeds during CDT were identified by cellular ultrastructural analysis, whole-body optical imaging, Western blotting and semi-quantitative RT-PCR. The alteration in mitochondrial morphology was an early event during CDT, as indicated by progressive dynamic mitochondrial changes and rupture of the mitochondrial outer membrane; loss of mitochondrial transmembrane potential (Δψ(m)) ensued, and mitochondrial ATP levels decreased. The mitochondrial permeability transition pore inhibitor cyclosporine A effectively suppressed these changes during ageing. The in situ localization of production of reactive oxygen species (ROS), and evaluation of the expression of voltage-dependent anion-selective channel and cyclophilin D indicated that the levels of mitochondrial permeability transition pore components were positively correlated with ROS production, leading to an imbalance of the cellular redox potential and ultimately to programmed cell death. Pre-incubation with ascorbic acid slowed loss of mitochondrial Δψ(m), and decreased the effect of CDT on seed viability. However, there were no significant changes in multiple antioxidant elements or chaperones in the mitochondria during early stages of ageing. Our results indicate that CDT induces dynamic changes in mitochondrial physiology via increased ROS production, ultimately resulting in an irreversible loss of seed viability.
authors.affiliation: National Engineering Laboratory for Tree Breeding, College of Biological Sciences and Biotechnology, Beijing Forestry University, 35 Tsinghua East Road, Beijing, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Li
authors.forename: Hua
authors.initials: H
authors.lastname: Xue
authors.forename: Hugh W
authors.initials: HW
authors.lastname: Pritchard
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Wang
mesh_terms: D016923:Cell Death / Q000235:genetics / Q000502:physiology; D000081406:Peptidyl-Prolyl Isomerase F; D021983:Cyclophilins / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000378:metabolism* / Q000502:physiology / Q000648:ultrastructure; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012639:Seeds / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D034403:Ulmus / Q000166:cytology / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D050994:Voltage-Dependent Anion Channels / Q000378:metabolism
chemical_list: D000081406:Peptidyl-Prolyl Isomerase F; D017382:Reactive Oxygen Species; D050994:Voltage-Dependent Anion Channels; D021983:Cyclophilins
keywords: controlled deterioration treatment; elm seed (Ulmus pumila L.); mitochondria; mitochondrial permeability transition pore; programmed cell death; reactive oxygen species