Methyl jasmonate induces production of reactive oxygen species and alterations in mitochondrial dynamics that precede photosynthetic dysfunction and subsequent cell death.
Methyl jasmonate (MeJa) is a well-known plant stress hormone. Upon exposure to stress, MeJa is produced and causes activation of programmed cell death (PCD) and defense mechanisms in plants. However, the early events and the signaling mechanisms of MeJa-induced cell death have yet to be fully elucidated. To obtain some insights into the early events of this cell death process, we investigated mitochondrial dynamics, chloroplast morphology and function, production and localization of reactive oxygen species (ROS) at the single-cell level as well as photosynthetic capacity at the whole-seedling level under MeJa stimulation. Our results demonstrated that MeJa induction of ROS production, which first occurred in mitochondria after 1 h of MeJa treatment and subsequently in chloroplasts by 3 h of treatment, caused a series of alterations in mitochondrial dynamics including the cessation of mitochondrial movement, the loss of mitochondrial transmembrane potential (MPT), and the morphological transition and aberrant distribution of mitochondria. Thereafter, photochemical efficiency dramatically declined before obvious distortion in chloroplast morphology, which is prior to MeJa-induced cell death in protoplasts or intact seedlings. Moreover, treatment of protoplasts with ascorbic acid or catalase prevented ROS production, organelle change, photosynthetic dysfunction and subsequent cell death. The permeability transition pore inhibitor cyclosporin A gave significant protection against MPT loss, mitochondrial swelling and subsequent cell death. These results suggested that MeJa induces ROS production and alterations of mitochondrial dynamics as well as subsequent photosynthetic collapse, which occur upstream of cell death and are necessary components of the cell death process.
MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, South China Normal University, Guangzhou 510631, PR China.
Lingrui
L
Zhang
Da
D
Xing
D000085:Acetates / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology; D017360:Arabidopsis / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*; D016923:Cell Death / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002736:Chloroplasts / Q000187:drug effects / Q000378:metabolism; D003517:Cyclopentanes / Q000494:pharmacology*; D016572:Cyclosporine / Q000494:pharmacology; D005453:Fluorescence; D049452:Green Fluorescent Proteins / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism*; D008933:Mitochondrial Swelling / Q000187:drug effects; D012275:Oryza / Q000187:drug effects / Q000378:metabolism; D054883:Oxylipins / Q000494:pharmacology*; D010788:Photosynthesis / Q000187:drug effects*; D011523:Protoplasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D036226:Seedlings / Q000187:drug effects / Q000378:metabolism; D013347:Subcellular Fractions / Q000187:drug effects; D013997:Time Factors; D031307:Vicia faba / Q000187:drug effects / Q000378:metabolism
D000085:Acetates; D000975:Antioxidants; D003517:Cyclopentanes; D054883:Oxylipins; D017382:Reactive Oxygen Species; D049452:Green Fluorescent Proteins; D016572:Cyclosporine; C072239:methyl jasmonate