Differential Sensitivities of Photofunctions of Thylakoid Membranes to Invivo Elevated Temperature Stress in Oryza Sativa (Var. Kalinga III) Seedlings

Abstract

Heat treatment (HT) of leaves, isolated chloroplasts or intact plants, causes inhibition of electron transport activities of both PSII and PSI (1). The order of thermal sensitivity of various photosynthetic light reactions is oxygen evolution, photochemical activity of PSII, Photophosphorylation, Cyt b6/f complex and photochemical activity of PSI (2). In vitro studies with isolated thylakoids suggest that loss of extrinsic protein namely 33 KDa Mn-stabilizing protein at the donor side of PSI1 and subsequent loss of Mn are the primary causes of inhibition of electron transport by heat stress (3). However, unlike the donor side, very few reports exist on the heat induced changes in the PSII acceptor side. Further, Michalski and Wettern,(4) observed that incubation of algal cells at 41.5 °C for 90 min resulted in membrane bound break down products of Dl-Polypeptide of 27 and 25 KDa. They suggest that heat shock might have led to these intermediates as a result of a heat-dependent inactivation of a protesase that degrades damaged Dl. They also reported that, D1 igestion during heat shock incubation in darkness resulted in an additional membrane bound intermediate of 15 KDa. Heat shock incubation in the presence of light did not induce any degradation products of D2 while treatment in dark led to the formation of two degradation products of 26 KDa. These results prompted us to study the degradation pattern of D1 and D2 upon in vivo HT in higher plants and also QA to QB electron transfer to ascertain changes if any. Most of the studies relating to heat stress deal with in vitro experiments using isolated chloroplasts or PSII/PSI sub-membrane fractions. Therefore, it was felt necessary to study stress response of PSII in in vivo.