Photoinhibition

Photoinhibition is light-induced reduction in the photosynthetic capacity of a plant, alga, or cyanobacterium. Photosystem II (PSII) is more sensitive to light than the rest of the photosynthetic machinery, and most researchers define the term as light-induced damage to PSII. In living organisms, photoinhibited PSII centres are continuously repaired via degradation and synthesis of the D1 protein of the photosynthetic reaction center of PSII. Photoinhibition is also used in a wider sense, as dynamic photoinhibition, to describe all reactions that decrease the efficiency of photosynthesis when plants are exposed to light. Photoinhibition is light-induced reduction in the photosynthetic capacity of a plant, alga, or cyanobacterium. Photosystem II (PSII) is more sensitive to light than the rest of the photosynthetic machinery, and most researchers define the term as light-induced damage to PSII. In living organisms, photoinhibited PSII centres are continuously repaired via degradation and synthesis of the D1 protein of the photosynthetic reaction center of PSII. Photoinhibition is also used in a wider sense, as dynamic photoinhibition, to describe all reactions that decrease the efficiency of photosynthesis when plants are exposed to light. The first measurements of photoinhibition were published in 1956 by Bessel Kok. Even in the very first studies, it was obvious that plants have a repair mechanism that continuously repairs photoinhibitory damage. In 1966, Jones and Kok measured the action spectrum of photoinhibition and found that ultraviolet light is highly photoinhibitory. The visible-light part of the action spectrum was found to have a peak in the red-light region, suggesting that chlorophylls act as photoreceptors of photoinhibition. In the 1980s, photoinhibition became a popular topic in photosynthesis research, and the concept of a damaging reaction counteracted by a repair process was re-invented. Research was stimulated by a paper by Kyle, Ohad and Arntzen in 1984, showing that photoinhibition is accompanied by selective loss of a 32-kDa protein, later identified as the PSII reaction center protein D1. The photosensitivity of PSII from which the oxygen evolving complex had been inactivated with chemical treatment was studied in the 1980s and early 1990s. A paper by Imre Vass and coworkers in 1992 described the acceptor-side mechanism of photoinhibition. Measurements of production of singlet oxygen by photoinhibited PSII provided further evidence for an acceptor-side-type mechanism. The concept of a repair cycle that continuously repairs photoinhibitory damage, evolved and was reviewed by Aro et al. in 1993. Many details of the repair cycle, including the finding that the FtsH protease plays an important role in the degradation of the D1 protein, have been discovered since. In 1996, a paper by Tyystjärvi and Aro showed that the rate constant of photoinhibition is directly proportional to light intensity, a result that opposed the former assumption that photoinhibition is caused by the fraction of light energy that exceeds the maximum capability of photosynthesis. The following year, laser pulse photoinhibition experiments done by Itzhak Ohad's group led to the suggestion that charge recombination reactions may be damaging because they can lead to production of singlet oxygen. The molecular mechanism(s) of photoinhibition are constantly under discussion. The newest candidate is the manganese mechanism suggested 2005 by the group of Esa Tyystjärvi. A similar mechanism was suggested by the group of Norio Murata, also in 2005. Photoinhibition occurs in all organisms capable of oxygenic photosynthesis, from vascular plants to cyanobacteria. In both plants and cyanobacteria, blue light causes photoinhibition more efficiently than other wavelengths of visible light, and all wavelengths of ultraviolet light are more efficient than wavelengths of visible light. Photoinhibition is a series of reactions that inhibit different activities of PSII, but there is no consensus on what these steps are. The activity of the oxygen-evolving complex of PSII is often found to be lost before the rest of the reaction centre loses activity. However, inhibition of PSII membranes under anaerobic conditions leads primarily to inhibition of electron transfer on the acceptor side of PSII. Ultraviolet light causes inhibition of the oxygen-evolving complex before the rest of PSII becomes inhibited. Photosystem I (PSI) is less susceptible to light-induced damage than PSII, but slow inhibition of this photosystem has been observed. Photoinhibition of PSI occurs in chilling-sensitive plants and the reaction depends on electron flow from PSII to PSI. Photosystem II is damaged by light irrespective of light intensity. The quantum yield of the damaging reaction in typical leaves of higher plants exposed to visible light, as well as in isolated thylakoid membrane preparations, is in the range of 10−8 to 10−7 and independent of the intensity of light. This means that one PSII complex is damaged for every 10-100 million photons that are intercepted. Therefore, photoinhibition occurs at all light intensities and the rate constant of photoinhibition is directly proportional to light intensity. Some measurements suggest that dim light causes damage more efficiently than strong light. The mechanism(s) of photoinhibition are under debate, several mechanisms have been suggested. Reactive oxygen species, especially singlet oxygen, have a role in the acceptor-side, singlet oxygen and low-light mechanisms. In the manganese mechanism and the donor side mechanism, reactive oxygen species do not play a direct role. Photoinhibited PSII produces singlet oxygen, and reactive oxygen species inhibit the repair cycle of PSII by inhibiting protein synthesis in the chloroplast. Strong light causes the reduction of the plastoquinone pool, which leads to protonation and double reduction (and double protonation) of the QA electron acceptor of Photosystem II. The protonated and double-reduced forms of QA do not function in electron transport. Furthermore, charge recombination reactions in inhibited Photosystem II are expected to lead to the triplet state of the primary donor (P680) more probably than same reactions in active PSII. Triplet P680 may react with oxygen to produce harmful singlet oxygen. If the oxygen-evolving complex is chemically inactivated, then the remaining electron transfer activity of PSII becomes very sensitive to light. It has been suggested that even in a healthy leaf, the oxygen-evolving complex does not always function in all PSII centers, and those ones are prone to rapid irreversible photoinhibition. A photon absorbed by the manganese ions of the oxygen-evolving complex triggers inactivation of the oxygen-evolving complex. Further inhibition of the remaining electron transport reactions occurs like in the donor-side mechanism. The mechanism is supported by the action spectrum of photoinhibition. Inhibition of PSII is caused by singlet oxygen produced either by weakly coupled chlorophyll molecules or by cytochromes or iron-sulfur centers.