Abstract

Exposure of plants to light intensities higher than those required to saturate photosynthesis leads to a reduction in photosynthetic capacity. This effect is known as photoinhibition. Photoinhibition is followed by destruction of carotenoids, bleaching of chlorophylls and increased lipid peroxidation due to damage by oxygen‐derivatives. The oxygen concentration in chloroplasts in the light is high because of oxygen production by photosystem II (PSII). This can result in the release of reactive intermediates of reduced dioxygen such as superoxide radicals, hydroxyl radicals, hydrogen peroxide or singlet oxygen. In order to maintain their normal function under light stress conditions, chloroplasts have developed multiple repair and protection systems. The induction of specific light stress proteins, the ELIPs (for early light‐induced proteins) can be considered to be part of these protective responses. The accumulation of ELIPs under light stress conditions is correlated with the photoinactivation of PSII, degradation of the Dl‐protein of PSII reaction centre and changes in the level of pigments. Futhermore, the accumulation of ELIPs in the thylakoids is strictly controlled by the pigment content, especially by chlorophylls. Isolation of ELIPs in a native form and analysis of pigments bound to these proteins revealed that ELIPs can bind chlorophyll a and lutein. These data indicate that ELIPs might represent unique chlorophyll‐binding proteins which have a transient function(s) during light stress. A transient ‘pigment‐carrier’ function is postulated for ELIPs.

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