Interaction Between Light And Water Stress In Plants Biology Essay

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In addition to the association with heat stress, high light conditions are frequently correlated with water deficit in the fields, 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 photosynthesis 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. On the other hand, 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, repair is 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 measured from isolated membranes (Takahashi and Murata 2008). Recent evidence confirms that photoinhibition is directly related to D1 protein damage and recovery, and D1 protein damage leads to a decrease in electron transfer or an increase in 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 accelerated the decline of electron transfer during high irradiance treatment, their dephosphorylation increased the susceptibility of the thylakoid membranes to the photoinhibitory treatment. Rintamaki et al. (1995) reported that the degradation of the D1 protein 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 reduce oxidative damage to the photosystems 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 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. The best studied biochemical protective mechanism is the non-photochemical quenching of excitation energy. Visible light-induced photoinhibition is ~25 % faster in an Arabidopsis thaliana mutant 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 exposure 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 consists of 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 grown in strong light. However, environmental stresses such as extreme temperatures, salinity and drought limit the supply of CO2 for use in CO2 fixation, which decreases the rate of repair of PS II (Takahashi and Murata 2008). The PS II repair cycle is based on the recycling of PS II subunits (except for the D1 protein) from the inhibited unit to the repaired one.