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Plant and Cell Physiology Advance Access published online on June 5, 2008

Plant and Cell Physiology, 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 e-mail: 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, China

Corresponding author: Prof. Da Xing. MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, South China Normal University, Guangzhou 510631, China, Telephone: +86-20-8521-0089, Fax: +86-20-8521-6052, Email: xingda{at}scnu.edu.cn


   Abstract

Methyl jasmonate (MeJa) is a well-known plant stress hormone. Upon exposure to stress, MeJa is produced and cause 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 mitochondria dynamics, chloroplasts 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 stimuli. Our results demonstrated that MeJa induction of ROS production, which firstly occurred in mitochondria after 1 h MeJa treatment and subsequently in chloroplasts by the time of 3 h treatment, caused a series of alterations in mitochondrial dynamics including the cessation of mitochondria movement, the loss of mitochondria transmembrane potential (MPT), and the morphology transition and aberrant distribution of mitochondria. Thereafter, photochemical efficiency dramatically declined before obvious distortion in chloroplasts morphology, which is prior to MeJa-induced cell death in protoplasts or intact seedlings. Moreover, treatment of protoplast with ascorbic acid (AsA) or catalase (CAT) prevented ROS production, organelle change, photosynthetic dysfunction and subsequent cell death. The permeability transition pore inhibitor cyclosporin A (CsA) gave significant protection against MPT loss, mitochondrial swelling, and subsequent cell death. These results suggested that MeJa induces ROS production and mitochondrial dynamics alterations as well as subsequent photosynthetic collapse, which occur upstream of cell death and are necessary components of cell death process.

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

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