Temperature Stress and Redox Homeostasis: The Synergistic Network of Redox and Chaperone System in Response to Stress in Plants

A remarkable number of strategies has been developed by living organisms to mitigate conflict with environmental changes. The global environment rising with ambient temperature has a wide range of effects on plant growth, and therefore activation of various molecular defenses before the appearance of heat damage. Evidence revealed key components of stress that trigger enhanced tolerance, and some determinants for plant tolerance have been identified. The interplay between heat shock proteins (HSP) and redox proteins is supposed to be vital for the survival under extreme stress conditions. Any circumstance in which cellular redox homeostasis is disrupted can lead to the generation of reactive oxygen species (ROS) that are continuously generated in cells as an unavoidable consequence of aerobic life. Integrative network analysis of synthetic genetic interactions, protein-protein interactions, and functional annotations revealed many new functional processes linked to heat stress (HS) and oxidative stress (OS) tolerance, implicated upstream regulators activated by the either HS or OS, and revealed new connections between them. We present different models of acquired stress resistance to interpret the condition-specific involvement of genes. Considering the basic concepts and the recent advances, the following subsections provide an overview of calcium ion (Ca2+) and ROS interplay in abiotic signaling pathways; further we introduce several examples of chaperone and redox proteins that respond the change of cellular redox status under environmental circumstances. Thus, the involvement or contribution of redox proteins through the functional switching in conjunction with the HSP that prevent heat- and oxidative-induced protein aggregation in plants.