Heat Stress: Susceptibility, Recovery and Regulation

The primary targets of thermal damage in plants are the oxygen-evolving complex and its associated cofactors in photosystem II (PS II), carbon fixation by Rubisco (Ribulose-1,5-bisphosphate carboxylase oxygenase) and the ATP generating system. The enzyme Rubisco activase is extremely sensitive to weak and moderate heat stress. Recent investigations on the combined action of moderate light intensity and heat stress suggest that moderately high temperatures do not cause serious PS II damage but inhibit the repair of PS II. The latter largely involves de novo synthesis of proteins, particularly the D1 protein of the photosynthetic machinery that is damaged due to generation of reactive oxygen species (ROS), resulting in reduced rates of carbon fixation and oxygen evolution, as well as disruption of linear electron flow. The attack of ROS during moderate heat stress principally affects the repair system of PS II, but not directly the PS II reaction center. Heat stress additionally induces cleavage and aggregation of reaction center proteins and pigment-protein complexes, the mechanisms of such processes are as yet unclear. On the other hand, membrane-linked sensors seem to trigger the accumulation of compatible solutes like glycinebetaine in the neighborhood of PS II in thylakoid membranes. They also induce the expression of stress proteins that alleviate the ROS-mediated inhibition of stress damage repair of the photosynthetic machinery and are required for the acclimation process. In this chapter we summarize recent progress in the studies of molecular mechanisms involved during moderate heat stress on the photosynthetic machinery, especially in PS II and the CO2 assimilation system. We also examine joint effects of high temperature and other stress factors.