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ABSTRACT Inhibition of the net photosynthetic CO 2 assimilation rate ( P n ) by high temperature was examined in oak ( Quercus pubescens L.) leaves grown under natural conditions. Combined measurements of gas exchange and chlorophyll (Chl) a fluorescence were employed to differentiate between inhibition originating from heat effects on components of the thylakoid membranes and that resulting from effects on photosynthetic carbon metabolism. Regardless of whether temperature was increased rapidly or gradually, P n decreased with increasing leaf temperature and was more than 90% reduced at 45 °C as compared to 25 °C. Inhibition of P n by heat stress did not result from reduced stomatal conductance ( g s ), as heat‐induced reduction of g s was accompanied by an increase of the intercellular CO 2 concentration ( C i ). Chl a fluorescence measurements revealed that between 25 and 45 °C heat‐dependent alterations of thylakoid‐associated processes contributed only marginally, if at all, to the inhibition of P n by heat stress, with photosystem II being remarkably well protected against thermal inactivation. The activation state of ribulose‐1,5‐bisphosphate carboxylase/oxygenase (Rubisco) decreased from about 90% at 25 °C to less than 30% at 45 °C. Heat stress did not affect Rubisco per se , since full activity could be restored by incubation with CO 2 and Mg 2+ . Western‐blot analysis of leaf extracts disclosed the presence of two Rubisco activase polypeptides, but heat stress did not alter the profile of the activase bands. Inhibition of P n at high leaf temperature could be markedly reduced by artificially increasing C i . A high C i also stimulated photosynthetic electron transport and resulted in reduced non‐photochemical fluorescence quenching. Recovery experiments showed that heat‐dependent inhibition of P n was largely, if not fully, reversible. The present results demonstrate that in Q. pubescens leaves the thylakoid membranes in general and photosynthetic electron transport in particular were well protected against heat‐induced perturbations and that inhibition of P n by high temperature closely correlated with a reversible heat‐dependent reduction of the Rubisco activation state.
Haldimann et al. (Thu,) studied this question.