Mild heat stress induces the expression of heat shock proteins (HSPs) that protect plants from death during damaging heat treatments. It was assumed that the appearance in the cell of denatured proteins triggers the expression of HSP; however, recent results show that protein denaturation is not a prerequisite for this process. In this work we discuss a hypothetical mechanism for activation under heat stress of HSP expression promoted by short-term elevation of cytosolic Ca2+ level. According to our hypothesis, a prolonged elevation of Ca2+ has a negative influence on HSP expression. Therefore, calcium is transported from the cytosol into intracellular compartments, including mitochondria. The Ca2+ entry into mitochondria is accompanied by hyperpolarization of the inner mitochondrial membrane and by the increased production of reactive oxygen species (ROS). The increased ROS production contributes to the activation of HSP expression under mild heat stress but leads to plant death under severe heat shock. Thus, mitochondria and, possibly, other organelles play the crucial role in determining life or death fate of heat-treated plant cells by controlling the cytosolic Ca2+ content and ROS production.
Russian Journal of Plant Physiology – Springer Journals
Published: Mar 7, 2014
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