Abstract

In the autumn, bud endodormancy in deciduous fruit trees is induced by short days or low temperatures. Once established, endodormancy is broken by the accumulation of low temperature days, although the precise conditions for this transition vary by species and cultivar. By comparing the reactions of buds of the same cultivar to different chilling periods, these studies identified several genes involved in dormancy phase transitions such as stress response-, cell cycle- and phytohormone-related genes. The actions of heat shock proteins (HSP) may be one of the mechanisms that plants use to survive unfavorable conditions during the bud dormancy stage. More specifically, HSP have chaperone activity that maintain proteins in their functional conformation and thereby prevent the degradation of proteins exposed to cold stress. Small HSPs (sHSPs) function as membrane stabilizers and reactive oxygen species (ROS) scavengers, as well as act synergistically with the antioxidant system. These small proteins also play a key role in maintaining membrane quality attributes, including fluidity and permeability under chilling stress. Membrane damage and ROS production are multifaceted adverse effects of cold injury in plants. The production and accumulation of HSPs can produce greater chilling injury tolerance during endodormancy, which suggests that these proteins play a central role in acquired tolerance to cold conditions.

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