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The dynamics of photosynthesis are associated with three different time scales, namely a rapid photoresponse (minutes), photoinhibition (hours), and photoadaptation (days). A light-induced adverse effect on a biomolecule is termed photodynamic damage. Photodynamic damage usually occurs via the formation of a triplet state of the sensitizing chromophore (Halliwell and Gutteridge 1999, Tyystjärvi 2004). PS II is a multiprotein complex that catalyzes the oxidation of H2O and reduction of Pq during photosynthesis (Iwata and Barber 2004) and susceptible to photoinhibition under visible and UV light (Melis 1999).
Several mechanisms have been suggested to explain the photoinhibition of PS II, including the over-reduction of the acceptor side of PS II, which was proposed to lead to the double reduction of the Pq electron acceptor, oxidative damage caused by sporadic inactivity of the donor-side of PSII (Anderson et al. 1998), and singlet oxygen production by uncoupled antenna Chls (Santabarbara et al. 2001, Adir et al. 2003). Photoinhibition of PS II had been proposed to be triggered by light-induced damage to the oxygen-evolving manganese (Mn) cluster (Onishi et al. 2005, Hakala et al. 2005). It is hypothesized that light absorption by the Mn (III) and/or Mn (IV) ions of the oxygen-evolving complex (OEC) leads to the release of a Mn ion from the OEC, which inhibits electron flow to the oxidized primary donor of PS II. Because photoinhibition mainly involves the photochemical inactivation of PS II, all photosynthesizing organisms suffer from damage by irradiation. However, the degree of susceptibility to photodamage is differently influenced by several types of factors: environmental (light intensity, temperature, water status, CO2 and O2 concentration, and soil fertility), genotypical (sun or shade plants), phenotypical (bending status of leaves), and physiological (carbon metabolism) factors. In general, the imposition of additional stress factors during exposure of a stressful factor in photosynthetic activity exacerbates the adverse effects.
Interaction between light and ambient CO2
Lack of CO2 and low CO2 partial pressure causes photoinhibition in C3 plants that depends on the intensity and length of light exposure. Photoinhibition was also found to be prevented to a great extent by partial O2 pressure in C3 plants; photoinhibition of PS II differs from typical reactions of types I and II, as PS II is readily inactivated in the absence of oxygen (Hakala et al. 2005). As O2 participates in carbon metabolism through the photorespiratory carbon oxidation (PCO) cycle, both O2 and CO2 can prevent photoinhibition by maintaining a low activity of carbon metabolism in light. Under CO2-limiting conditions, Ribulose-1,5-biphosphate carboxylase/oxygenase (Rubisco) catalyzes the oxygenation of ribulose-1,5-biphosphate (RuBP) to produce glycolate-2-P to the Calvin cycle intermediate glycerate-3-P and is proposed to be important for avoiding photoinhibition of PS II, especially in C3 plants (Takahashi et al. 2007). During this PCO cycle, ammonia and CO2 are produced by the mitochondrial Gly decarboxylase. Ammonia is subsequently refixed into Glu by plastidic isozymes of Gln synthetase and Fd-dependent Glu synthase in the photorespiratory nitrogen cycle (Linka and Weber 2005). Thus, the photorespiratory pathway consists of the photorespiratory carbon and nitrogen cycles (Takahashi and Badger 2010). Impairment of the photorespiratory pathway interrupts photosynthetic CO2 fixation (owing to the lack of Calvin cycle metabolites and accumulation of photorespiratory pathway intermediates that inhibit the Calvin cycle) and accelerates photoinhibition (Kozaki and Takeba 1996, Melis 1999 and Takahashi et al. 2007). On the other hand, Li et al. (2008) suggested that elevated [CO2] could increase photochemical efficiency under drought stresses and be beneficial to cucumber seedling in drought environment, thus alleviate or offset the negative consequences of global environmental changes.
Interaction between light and temperature stress
Photosynthesis is one of the first processes affected by low temperatures. Exposure of plants to cool (12°C) or freezing (<0°C) temperatures sometimes produces adverse effects on their metabolic functions. Remarkably, the symptoms of low-temperature damage to the photosynthetic apparatus are particularly evident when substantial light follows exposure to low temperature. The main site of photoinhibition at low temperatures is not PS II but PS I (Sonoike 1999). Hydroxyl-radicals destroy the FeS centers as well as a PS I reaction center subunit, the PsaB protein (Terashima et al. 1998). However, the biochemical mechanism(s) of the interactive effect of cool temperatures and moderate light intensity on photosynthetic activity has not been yet fully elucidated. In relation to this, Venema et al. (2000) showed that the degradation of leaf pigments was slower in plants grown at suboptimal temperatures than in plants grown at optimal temperatures when Lycopersicon species was subjected to light of 1000 ïmol m-2s-1 at 5°C for two days. As well, non-photochemical quenching of Chl fluorescence was higher in leaves of sub-optimally grown plants, which presented xanthophyll cycle pigments in a larger pool. These mean that acclimation to sub-optimal temperatures increases the capacity to resist chill-induced photodamage. On the other hand, Havaux and Tardy (1996) noticed that treatment of Lycopersicon esculentum leaves at 35°C for two hours induced a tolerance of PS II to light as well as to temperatures above 40°C. They confirmed that a short exposure of L. esculentum leaves to a light of 1000 ïmol m-2s-1 during four minutes significantly increased the thermostability of PS II as a function of temperature.
As one of the biochemical mechanisms on damage of photosynthesis by the interaction between light and temperature stress, researchers have proposed that particular lipid structures have crucial roles in ensuring proper photosynthetic function (Siegenthaler and Murata 1998). Several lines of evidence indicate that thylakoid fatty-acid composition influences photoinhibition. Damage to D1 is directly proportional to light intensity (Tyystjärvi and Aro, 1996), and inactivated protein molecules must be replaced by newly synthesized D1 proteins to restore PS II activity (Kanervo et al. 1997, Kettunen et al. 1997, van Wijk et al. 1997, Zhang et al. 1999, 2000). In higher plants, the extent of low-temperature photoinhibition has been correlated with the level of saturated fatty acids (16:0 and 18:0) and of 16:1 (3-trans) in phosphatidylglycerol (PG) (Moon et al. 1995). Wild-type tobacco (Nicotiana tabacum) plants contain 67% of these fatty acids in leaf PG, but in a transgenic line expressing a squash (Cucurbita pepo) acyl-ACP:glycerol-3-P acyltransferase (Rbcs-SQ), the proportion was increased to 88% (Moon et al. 1995). Additional experiments demonstrated that the recovery process (rather than D1 damage) was affected in Rbcs-SQ plants at 17°C and 25°C. The implication is that delayed recovery from photoinhibition may be directly linked to the fatty acid composition of the chloroplast PG (Somerville, 1995). A series of lipid mutants available in Arabidopsis have provided important information about the relationship between lipid structure and membrane function (McConn and Browse 1998), and the effect of altering thylakoid fatty acid composition on damage and recovery processes during photoinhibition.
Interaction between light and water stress (drought)
In addition to the association with heat stress, light conditions are frequently correlated with water deficit in the natural field, or rather water stress is generally correlated with heat stress. Plants respond to water stress by stomatal response, which regulates CO2 availability in the chloroplasts, and thus photosynthesis and photosynthetic capacity are governed under drought. In consequence, a lower light intensity is required to saturate photosynthesis under drought than under well-watered conditions (Lawlor 1995). Water stress affects both stomatal conductance and photosynthetic activity in the leaf (Goh et al. 1997, 1999, 2001, 2002). Therefore, the effect of water stress on photosynthetic activity has a stomatal component (restricted availability of CO2) and a non-stomatal component (direct inhibition of photosynthesis). Plant growth in elevated [CO2] reduce the benefits under water deficits, when elevated [CO2] is applied for several days or weeks and sometimes even a suppression of photosynthesis occurs (Sawada et al. 2001). Although there are many studies on photosynthetic responses to CO2 enrichment as well as to drought stress, there is yet limited quantitative understanding of the effects of interactions between CO2 and water deficiency (Widodo et al. 2003). Munne-Bosch and Alegre (2000) show that the efficiency of PS II photochemistry decreased to approximately 65% in plants exposed to high light and drought. Exceptionally, Havaux (2005) indicate that water stress enhanced the resistance of PS II to otherwise photoinhibitory conditions, such as heat or high light in several plant species.
5. The photoprotection and recovery of photoinhibition
The recovery of photoinhibition is observed even in time scales (Fig. 5). In photoinhibition studies, the biochemical processes of repair are often stopped by applying antibiotics (chloramphenicl, lincomycin, and etc) to plants, which blocks protein synthesis in the chloroplast. Protein synthesis only occurs in an intact sample, indicating that lincomycin is not needed when photoinhibition is occurred from the isolated membranes (Takahashi and Murata 2008). Recent evidence confirms that photoinhibition is directly related to D1 protein damage. As the result, it decreases the photosynthetic electron transfer or increases the turnover time of the electron transport chain. Studies addressing the recovery from photoinhibition established a role for D1 protein loss in photoinhibition. Exposure of leaves to moderate light and chilling temperatures led to selective photodamage of PS II in tropical trees grown under high light (Huang et al. 2010). After short-term chilling treatment under high light, PS II photodamage was quickly repaired under low light in several hours (He and Chow 2003, Zhang and Scheller 2004, Huang et al. 2010). This capacity for fast repair is due to the fast turnover rate of the D1 protein and the ability to repair and reuse damaged PS II subunits for the assembly of the PS II complex. The fast synthesis of the D1 protein and the repair of the damaged PS II subunits require a large amount of ATP in a short time (Allakhverdiev et al. 2005); however, the damage to PS II can decrease the linear electron flow (LEF) and therefore reduce the rate of synthesis of ATP, which needs to be synthesized through other pathways. One possible alternative pathway for ATP synthesis is the stimulation of cyclic electron flow around PS I during the recovery of PS II. This indicates that the recovery of PS II activity is not possible if PS I is severely photodamaged (Huang et al. 2010), but the exact role of PS I stability in the fast repair of PS II is unclear. The activity of PS I involves two modes of electron flow, namely linear electron flow and cyclic electron flow. Cyclic electron flow (CEF) around PS I helps build the trans-thylakoid membrane proton gradient, and favors the synthesis of ATP (Bendall and Manasse 1995) and the recovery of PS II (Allakhverdiev et al. 2005). CEF is likely stimulated during the recovery from photoinhibition to increase the synthesis of ATP. Severe damage to PS I would therefore inhibit the stimulation of CEF and inhibit ATP synthesis, therefore blocking the recovery of PS II.
Several studies indicate that photoinhibition of PS II is inversely proportional to the phosphorylation level of PS II proteins. While the phosphorylation of polypeptides induced the decline of electron transfer during high light treatment, their dephosphorylation increased the susceptibility of the thylakoid membranes to the photoinhibitory treatment. Rintamaki et al. (1995) reported that the D1 protein degradation of Cucurbita pepo subjected to photoinhibitory treatment was followed by the accumulation of phosphorylated D1, suggesting the involvement of phosphorylation in the regulation of D1 degradation, and therefore in the PS II repair cycle.
The mechanisms underlying the avoidance or tolerance of the photoinhibition of photosynthesis are speculated to involve morphological mechanisms such as leaf and cellular chloroplast movement (Goh et al. 2009). Leaves move to minimize the absorption of excessive light, and chloroplasts change their position to minimize the absorption of light (Takahashi and Badger 2010). Damaging radiation (UV and visible light) is also screened out by phenolic compounds in the cells of the epidermis (Takahashi and Badger 2010).
Formate is possibly involved in endogenous radical scavenging and/or in the supply of CO2 (derived from formate), which decrease the oxidative damage to the photosystems (PS II and PS I) under photoinhibitory conditions. Shiraishi et al. (2000) found that the application of potassium formate (at 2 mM) before photoinhibitory treatment protected rice leaves from photoinhibition.
Another strategy for minimizing the photoinhibition of PS II is the thermal energy dissipation of absorbed light energy (qE) (Takahashi and Badger 2010). The qE dissipates light energy absorbed by photosynthetic pigments by generating heat at minor light-harvesting proteins. Cyclic electron flow (CEF) around PS I can also avoid photoinhibition (Takahashi and Badger 2010). CEF includes both the NAD(P)H dehydrogenase complex-dependent and PGR5-dependent pathways and helps to generate ï„pH across the thylakoid membrane. Rapid photoinhibition caused by impairment of the photorespiratory pathway in Arabidopsis mutants has been attributed to the inhibition of the repair of photodamaged PS II (but not to the acceleration of photodamage to PS II) owing to the suppression of the de novo synthesis of the D1 protein at the translation step (Melis 1999). Because a block in photosynthetic CO2 fixation causes an imbalance between the amount of light energy absorbed and the plant's capacity for its utilization, inhibition of protein synthesis by impairment of the photorespiratory pathway can be attributed directly to the effects of excessive light such as ROS generation (Melis 1999, Takahashi and Murata 2006). Therefore, the activity of the photorespiratory pathway can limit the inhibition of the repair of photodamaged PS II by maintaining the energy utilization of the Calvin cycle, which reduces the generation of ROS when the supply of CO2 is limited (Takahashi and Badger 2010). The xanthophyll cycle plays a crucial role in the protection of plants from photoinhibition in light. Plants have mechanisms that protect them against the adverse effects of strong light. One of the best studies of biochemical protective mechanism, it is the non-photochemical quenching process of excitation energy in the photochemical activity. Visible light-induced photoinhibition is about 25 % faster in an Arabidopsis thaliana transgenic plant lacking non-photochemical quenching than in the wild type (Krause and Jahns 2004). Turning or folding of the leaves, as is observed in Oxalis species in response to high light, also protects against photoinhibition.
Under conditions of excess light, the production of ROS is accelerated in both PS I and PS II in chloroplasts, but different ROS are produced by each photosystem. In PS I, electron transfer to oxygen causes the production of hydrogen peroxide (H2O2) via the superoxide anion radical (O2-), while in PS II, the excitation of oxygen by triplet excited state chlorophyll (3Chl*) causes the production of singlet oxygen (1O2) (Asada 2006). To avoid oxidative stress, chloroplasts scavenge ROS effectively using multiple enzymes including superoxide dismutase, ascorbate peroxidase and peroxiredoxin, antioxidants such as the water-soluble ascorbate (Asada 2006) and membrane-bound a-tocopherol (Havaux et al. 2005), and carotenoids such as zeaxanthin (Havaux and Niyogi 1999), neoxanthin (Dall'Osto et al. 2007) and lutein (Peng et al. 2006) in chloroplasts. ROS are highly reactive and therefore accelerate photoinhibition through direct oxidative damage to PS II. However, recent studies have demonstrated that ROS, such as 1O2 and H2O2, accelerate photoinhibition through the inhibition of the repair of photo-damaged PS II rather than causing direct damage (Nishiyama et al. 2006).
The PS II repair cycle that takes place in chloroplasts is regulated by the degradation and synthesis of the D1 protein of the PS II reaction centers, followed by the activation of the reaction center. Due to the rapid repair process, most PS II reaction centers are not photoinhibited even if a plant is placed on strong light. However, environmental stresses such as extreme temperatures, salinity and drought limit the supply of CO2 for use in CO2 metabolism, which decreases the rate of PS II repair (Takahashi and Murata 2008). The PS II repair cycle is based on the recycling of PS II subunits from the inhibited unit to the repaired one.