Abstract
Different abiotic and biotic stresses lead to the production and accumulation of reactive oxygen species (ROS) in various cell organelles such as in mitochondria, resulting in oxidative stress, inducing defense responses or programmed cell death (PCD) in plants. In response to oxidative stress, cells activate various cytoprotective responses, enhancing the antioxidant system, increasing the activity of alternative oxidase and degrading the oxidized proteins. Oxidative stress responses are orchestrated by several phytohormones such as salicylic acid (SA). The biomolecule SA is a key regulator in mitochondria-mediated defense signaling and PCD, but the mode of its action is not known in full detail. In this review, the current knowledge on the multifaceted role of SA in mitochondrial ROS metabolism is summarized to gain a better understanding of SA-regulated processes at the subcellular level in plant defense responses.
Highlights
Surviving negative effects of a wide variety of environmental fluctuations is a substantial part of plant life
Detection of interactions between mitochondria, the ratio of active and inactive mitochondria, mitochondrial fusion and fission, and measurements upon salicylic acid (SA) can help to understand the role of SA in plant programmed cell death (PCD)
Tools of molecular biology can serve transgenic and mutant plants to describe the direct effects of SA on plant mitochondria
Summary
Surviving negative effects of a wide variety of environmental fluctuations is a substantial part of plant life. Genetic and morphologic changes of plants are necessary to acclimatize and/or adapt to harmful environmental conditions These changes are controlled by the rapid transient or chronic production and the scavenging of reactive oxygen species (ROS) [1,2,3]. The current knowledge on the multifaceted role of SA on mitochondrial ROS metabolism is collected and summarized in plants to gain a better understanding of SA-regulated processes at the physiological, biochemical and molecular levels. This knowledge can add a new aspect to the understanding of mitochondrial oxidative stress signaling and its crosstalk with plant immune responses
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