Damage of photosynthetic apparatus in the senescing basal leaf of Arabidopsis thaliana: a plausible mechanism of inactivation of reaction center II.

Significant decline in oxygen evolution and DCPIP photoreduction and a marginal restoration of the later with DPC as an electron donor suggest the inactivation of reaction center of photosystem II. The declines in the height of thermoluminescence bands support the view and the damage of reaction center II could be central to the senescence process in Arabidopsis leaves. The enhancement in the number of reduced quinones, signifying a loss in redox homeostasis in the electron transport chain between photosystem II and I leads to the creation of an energy imbalance. The view is supported by the decline in actual quantum yield of photosystem II in the light adapted state and maximum quantum yield of primary photochemistry in the dark adapted state of chlorophyll fluorescence. An increase in chlorophyll a fluorescence polarization and decline in carotenoid to chlorophyll energy transfer efficiency suggest the perturbation in thylakoid structure. A plausible mechanism illustrating the senescence mediated inactivation of oxygen evolving complex has been proposed.