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A daily occurrence in the life of a plant is the function of a photosystem II (PSII) damage and repair cycle in chloroplasts. This unique phenomenon involves the frequent turnover of D1, the 32-kDa reaction-center protein of PSII (chloroplast psbA gene product). In the model organism Dunaliella salina (a green alga), growth under low light (100 mol of photons per m2 per sec) entails damage, degradation, and replacement of D1 every 7 hr. Growth under irradiance stress (2200 micromol of photons per m2 per sec) entails damage to D1 every 20 min. The rate of de novo D1 biosynthesis under conditions of both low light and irradiance stress was found to be fairly constant on a per chloroplast or cell basis. The response of D. salina to the enhanced rate of damage entails an accumulation of photodamaged centers (80% of all PSII) and the formation of thylakoid membranes containing a smaller quantity of photosystem I (PSI) centers (about 10% of that in cells grown under low light). These changes contribute to a shift in the PSII/PSI ratio from 1.4:1 under low-light conditions to 15:1 under irradiance stress. The accumulation of photodamaged PSII under irradiance stress reflects a chloroplast inability to match the rate of D1 degradation or turnover with the rate of damage for individual PSII complexes. The altered thylakoid membrane organization ensures that a small fraction of PSII centers remains functional under irradiance stress and sustains electron flow from H2O to ferredoxin with rates sufficient for chloroplast photosynthesis and cell growth.

Photosystem II reaction center damage and repair cycle: chloroplast acclimation strategy to irradiance stress.