Abstract

Excessively high light intensities are damaging to the photosynthetic apparatus. Photosynthetic organisms are therefore faced with the problem of maintaining sufficient excitation power under limiting light conditions whilst avoiding photodamage under high light conditions. The primary target for this photodamage is Photosystem II (PSII), which undergoes inhibition of its electron transport followed by irreversible damage to and degradation of the D~ and D 2 reaction centre polypeptides. This degradation is the initial event in a repair cycle of photodamaged complexes and is followed by protein synthesis and reassembly of functional PSII. This report will deal with recent information relevant to the molecular mechanisms of PSII electron transport impairment and of protein degradation, particularly the D I protein, and the chemical link between these two events. Data will be presented in support of the following sequence of reactions (Fig. 1), which take place at PSII under high-light stress: (i) overreduction of the acceptor side, leading to the formation of stably reduced QA species; (ii) these events facilitate the formation of chlorophyll triplets which react with molecular oxygen to form singlet oxygen; (iii) this highly reactive and damaging species will oxidize pigments and/or amino-acid residues leading to irreversible damage to the reaction centre, mainly to the D l protein; (iv) the oxidative damage induces a conformational change in the D~ protein which triggers it for

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