Abstract

Mitogen-activated protein kinase (MAPK) cascades are evolutionarily conserved modules among eukaryotic species that range from yeast, plants, flies to mammals. In eukaryotic cells, reactive oxygen species (ROS) has both physiological and toxic effects. Both MAPK cascades and ROS signaling are involved in plant response to various biotic and abiotic stresses. It has been observed that not only can ROS induce MAPK activation, but also that disturbing MAPK cascades can modulate ROS production and responses. This review will discuss the potential mechanisms by which ROS may activate and/or regulate MAPK cascades in plants. The role of MAPK cascades and ROS signaling in regulating gene expression, stomatal function, and programmed cell death (PCD) is also discussed. In addition, the relationship between Rboh-dependent ROS production and MAPK activation in PAMP-triggered immunity will be reviewed.

Highlights

  • Reactive oxygen species (ROS), including hydrogen peroxide (H2O2), hydroxyl radical (HO), singlet oxygen (1O2), and superoxide anion (O2−), are formed upon partial reduction of oxygen (O2)

  • Experimental results indicate that O2 deprivation leads to mitochondria-dependent ROS production in A. thaliana [36]

  • The authors suggested that low O2 stimulates mitochondrial ROS that moves to the cytoplasm to activate Mitogen-activated protein kinase (MAPK), leading to retrograde signaling between mitochondria and nucleus

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Summary

Introduction

Reactive oxygen species (ROS), including hydrogen peroxide (H2O2), hydroxyl radical (HO), singlet oxygen (1O2), and superoxide anion (O2−), are formed upon partial reduction of oxygen (O2). Maintenance of the reduced and oxidized glutathione ratio (GSH/GSSG) is critical for ROS homeostasis In contrast to their potentially harmful effects, ROS play an important role in regulating plant growth and development, and response to biotic or abiotic stresses. It has been observed that, on one hand, exogenous application of H2O2 or ozone activates components of MAPK cascades, and initiation of ROS signaling can lead to changes in MAPK cascades (Table 1; [34,35]), on the other hand, manipulating MAPK cascades results in initiation of ROS responses (Table 2; [34,35]). These observations indicate that MAPK cascades are complicated in both ROS signaling and responses

Activation and regulation of MAPK cascades by ROS
Regulation of ROS-related genes by MAPK cascades
ROS and MAPK cascades in HR-like cell death
ROS and MAPK cascades in spontaneous cell death
ROS and MAPK cascades in acute ozone-induced PCD
ROS and MAPK cascades in fumonisin B1- and sphingolipidinduced PCD
ROS and MAPK cascades in self-incompatibilily-induced PCD
Rboh-dependent ROS production and MAPK cascades in PAMP-triggered immunity
Regulation of stomatal function by MAPK cascades in ROS signaling
Concluding remarks and perspectives
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