Abstract

Heat tolerance of Arabidopsis thaliana (WT) and its mutants, crr2-2, lacking NADPH-dehydrogenase (Ndh-pathway), and pgr5, deficient in proton gradient regulation and/or ferredoxin-quinone-reductase (FQR-pathway), was studied from 30 to 46°C. Chlorophyll fluorescence revealed that thermal damage to photosystem II (PSII) was maximal in WT plants following short-term exposure of leaves to moderate or high temperature stress. Thermal stress impaired the photosynthetic electron flow at oxidizing and reducing sides of PSII. This was deduced from the transformation of temperature dependent OJIP to OKP patterns, changes in the relative amplitudes of K-step fluorescence rise and F(v)/F(o) ratio. The amplitude of the K-peak that corresponds to the magnitude of damage to the oxygen evolving complex (OEC) in crr2-2 mutants was about 50% of that observed in WT plants exposed to 46°C. The damage to OEC in pgr5 mutants was relatively smaller and thus their PSII complexes were more heat tolerant. P700 oxidation-reduction kinetics following heat-stress revealed that photosystem I (PSI) complexes remained oxidizable either with 10-ms multiple turn-over flashes or far-red illumination but the complementary cyclic electron flow around PSI (CEF) was abolished in both mutants. With further increase in incubation temperature, CEF was fully suppressed even in WT. Thus, P700 turn-over was not enhanced following thermal stress. Furthermore, the experimental data predicts the onset of pseudocyclic electron transport with molecular oxygen as terminal acceptor in crr2-2 and pgr5 mutants but not in wild type Arabidopsis subjected to severe thermal-stress.

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