Abstract

To examine whether damage to zooxanthellar photosystem II (PSII) is the primary step of thermally induced coral bleaching, we first assessed the relationship between the maximum quantum yield of PSII (Fv/Fm) or active PSII centers (Fv/Fo) and maximum electron transport rate (ETRmax), which represent the PSII activity and electron flow beyond the PSII, respectively, in the symbiotic algae of the coral Pachyseris rugosa. Next, the photo-physiological responses of the symbionts to stress treatments of 1h high temperature (33.5°C) and/or high light (1030μmol quanta m-2 s-1) stress and 6h recovery were investigated. The 1h high temperature treatment in darkness produced a significant, but reversible (6h recovery) decline in ETRmax without any change in Fv/Fm. The 1h high light treatment reduced Fv/Fm, but not ETRmax. High temperature in combination with high light resulted in a more pronounced reduction in Fv/Fm, along with a significant decline in ETRmax. Neither Fv/Fm nor ETRmax recovered fully within 6h. Reversible increases in non-photochemical quenching (NPQ), energy dissipation in PSII, were also recorded. Chloramphenicol (CAP), an inhibitor of synthesis of D1 protein of PSII reaction center, revealed that a minimum of -60% of the Fv/Fm or -30% of active PSII centers (Fv/Fo) is required to maintain ETRmax in the in hospite symbionts. These results suggest that the primary step of heat-induced damage in the symbiont's photosynthetic apparatus involves a component beyond the PSII, probably at the level of the dark reaction as indicated by reduced ETRmax and the PSII damage is secondary.

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