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Plant and Cell Physiology Advance Access originally published online on June 5, 2008
Plant and Cell Physiology 2008 49(7):1092-1111; doi:10.1093/pcp/pcn086
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© The Author 2008. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Methyl Jasmonate Induces Production of Reactive Oxygen Species and Alterations in Mitochondrial Dynamics that Precede Photosynthetic Dysfunction and Subsequent Cell Death

Lingrui Zhang and Da Xing*

MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, South China Normal University, Guangzhou 510631, PR China

*Corresponding author: E-mail, xingda{at}scnu.edu.cn; Fax, +86-20-8521-6052.


  Abstract

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.

Keywords: Cell death - Chloroplast - Methyl jasmonate - Mitochondrial dynamics - Photochemical efficiency - Reactive oxygen species

Abbreviations: AsA, ascorbic acid; CAT, catalase; CsA, cyclosporin A; DCF, dichlorofluorescein; DF, delayed fluorescence; DTT, dithiothreitol; ET, ethylene; FB1, fungal toxin fumonisin B1; FDA, fluorescein diacetate; GFP, green fluorescent protein; H2DCFDA, 2', 7'-dichlorodihydrofluorescein diacetate; H2O2, hydrogen peroxide; HR, hypersensitive response; Ja, jasmonic acid; LCSM, laser confocal scanning microscope; MeJa, methyl jasmonate; MO, methyl oleate; MPTP, mitochondrial permeability transition pore; MTP, mitochondrial transmembrane potential; PA, phytyl acetate; PCD, programmed cell death; PMSF, phenylmethylsulfonyl fluoride; Pn, net photosynthesis rate; Rh123, rhodamine 123; ROS, reactive oxygen species; Rubisco, ribulose bisphosphate carboxylase/oxygenase; SA, salicylic acid; SPCM, single photon counting module.

(Received May 11, 2008; Accepted June 2, 2008)
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