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Temperature is an abiotic environmental factor that significantly affects life processes in all organisms by modifying membrane properties, enzyme activity levels, the rate of chemical reactions and diffusion, viscosity of vacuole solution and the cytoplasm, phloem and xylem solutions in plants (e.g. Sung et al. 2003). Living organisms can be classified into three groups, subject to the preferred temperature of growth (Fig.1). This chapter analyzes the impact of temperature on plant growth with emphasis on plant response to temperature stress.
It is believed that land plants evolved in a tropical climate. This evolution process was spurred not so much by a warm climate, but by the stability of ambient temperature. Plants gradually migrated into temperate regions both north and south of the equator as they developed mechanisms that allowed them to accommodate wider variations in temperature on both a daily and a seasonal basis (Fitter and Hay 2002). The growth and development of plants involves a countless number of biochemical reactions that are sensitive to temperature. Plant life is generally limited by the freezing point of water at the low end of the temperature scale and the irreversible denaturation of proteins at the high end. Temperature is a critical factor in the plant environment, and it may play a significant role in growth and development. Growth is defined as an increase in dry weight, while development is the increase in the number and/or dimension of organs by cell division and/or expansion: leaves, branches, spikelets, florets, root apices etc., including those present in seed embryos. It also seems that the rate of plant development tends to be controlled primarily by temperature, and it is less sensitive to other environmental factors. The development of vegetation is determined by a broad variety of environmental factors that exert combined effects. Plant organisms are rarely affected by individual factors, and temperature stress is usually accompanied by water stress and, in consequence, oxidative stress (Fitter and Hay 2002). Temperature can also play a part in controlling the pattern and timing of plant development, and this accounts for the below phenomena:
In some plant species, a period of low temperatures is required to induce flowering, while in other plants, low temperatures only accelerate flowering or have no effect at all. Plants with a vernalization requirement experience a period of low temperatures in late fall and/or winter at the stage of seed imbibition or young seedlings (annual winter crops) or upon reaching vegetative maturity (biennial and perennial plants) (Kim et al. 2009). Flowering is induced in the temperature range of 0 to +10Â°C. The duration of the vernalization period, i.e. the required number of days with low temperatures, varies subject to species, and it usually reaches from two weeks to several weeks (Denis et al. 1996; Amasino 2006). In seeds, temperature stimuli are perceived by the embryo, while in seedlings and matured plants, this signal is sensed by apical meristems. A vernalized meristem retains competence following the reception of the inductive signal. When the signal is absent for a longer period of time, the plant is de-vernalized, and a similar effect can be achieved by exposing the plant to higher temperatures (around 40Â°C for 1-2 days) (Tretyn et al. 2003). The mechanisms underlying vernalization have not yet been fully explained. It is believed that low temperatures lead to changes in the permeability of cell membranes and/or the level of expression of "vernalization" genes. Phytohormones, in particular gibberellin, significantly contribute to this process (Sheldon et al. 2000; Amasino 2005).
Stratification is a popular method of breaking seed dormancy that has been used for centuries. This technique involves the storage of seeds in a moist and well ventilated environment at relatively low temperatures in the range of 1-10Â°C. Stratification is generally defined as the process of subjecting seeds to cold or warm and cold conditions in a moist and ventilated environment to break the dormancy stage. Low temperature, high moisture content and oxygen supply during the treatment induce deep physiological and biochemical changes in seeds. Stratification leads to the decomposition of germination inhibitors in seeds, and it induces the production of growth stimulators: cytokinin, gibberellin and auxin. At various stages of the dormancy breaking period, changes are noted in the quantitative ratio of various stimulators which modify the seeds' sensitivity to light and temperature and support dormancy breaking in various dormancy mechanisms (eg. Baskin and Baskin 1998, Opik and Rolfe 2005, Wróbel et al. 2005).
c) THE EFFECT OF TEMPERATURE ON MEMBRANES, ENZYMES AND METABOLIC PROCESSES
An increase or a decrease in temperature changes the kinetic energy of particles, accelerating their motion and weakening hydrogen bonds in macromolecules. All of the reactions contributing to growth are catalyzed by enzymes whose activity depends on their precise, three-dimensional, tertiary structures, to which the reacting molecules must bind exactly for each reaction to proceed. As the temperature rises, tertiary structures are damaged, reducing enzyme activity and reaction rates (Price and Stevens 1999). The asymmetry of response curves, such as Fig. 2, is the net result of an exponential increase in the reaction rate, caused by increased collision frequency, and increasingly modified by the thermal denaturation of macromolecules (Fitter and Hay 2002) .
The effect of temperature on enzyme activity is not a simple correlation. Activity levels rise with an increase in temperature, but only within a temperature range that guarantees the enzyme's stability (Cornish-Bowden 2004). When the critical temperature is exceeded, enzymes undergo thermal denaturation, and their activity drops rapidly. The average rate of enzymatic reactions increases two-fold with every 10Â°C increase in temperature within the range that does not cause enzyme denaturation (Fig. 3). The correlation between temperature and the increase in enzymatic activity is described by temperature coefficient Q10 which illustrates changes in reaction rate when the temperature increases by 10Â°C:
Parameter Q10 applies only in a non-denaturing range of temperatures, it is enzyme specific and determined by the activation energy of the catalyzed reaction. Enzyme activity reaches the highest level at optimal temperature. The representative values of temperature coefficients (Q10) for selected plant processes measured at varying intervals within the range 0-300C are determined at 1 - 2.3 (e.g. light reactions of photosynthesis ~ 1; diffusion of small molecules in water: 1.2-1.5; water flow through seed coat: 1.3-1.6; water flow into germinating seeds: 1.5-1.8; hydrolysis reactions catalyzed by enzymes: 1.5-2.3; root axis extension: 2.3). Coefficient value reaches 2-3 for dark reactions of photosynthesis, 0.8-3 for phosphate ion uptake into storage tissue and 2-5 for potassium ion uptake into seedlings. Grass leaf extension is characterized by Q10 of 3.2, and the relative growth rate is marked by coefficient value of 7.2 (Fitter and Hay 2002). The observed optimal temperature is the product of two processes: an increase in the reaction rate related to an increase in kinetic energy and an increase in the rate of thermal denaturation of an enzyme above a critical temperature point. When the second parameter is higher, a drop in activity levels is noted. For most enzymes, the optimal temperature falls within the range of 30-45Â°C. Enzymes are irreversibly denatured and inactivated at temperatures higher than 60Â°C. The enzymes of thermophilous organisms (such as thermal spring bacteria) remain active and attain maximum reaction rates at higher temperatures. The highest temperature at which an enzyme is not thermally inactivated under given conditions determines the enzyme's thermal stability.
An alternative approach involves the application of the Arrhenius equation (from chemical kinetics) to plant processes:
k = A exp ( -Ea/RT)
k - rate constant; Ea - activation energy for the process; A -constant; R -gas constant; T (temperature) - expressed on the absolute temperature scale
Arrhenius constants (Ea/R for the process) can be useful in biochemical comparisons between species (e.g. Criddle et al. 1994, Levine 2005) and in analyses of plant membrane changes during cooling and freezing.
Higher temperatures increase the liquidity of membrane lipid layers. A temperature drop has the opposite effect: biological membranes become more rigid and the activation energy of membrane enzymes increases. The above phenomenon is as the result of thermotropic changes in the lipid phase. Temperature modifies the organization of fatty acid residues in phospholipids and galactolipids, the components of various membranes. The configuration of polyunsaturated fatty acid residues is more difficult to reorganize at lower temperatures than that of saturated fatty acids, but polyunsaturated fatty acids residues "melt" more easily at higher temperatures. Temperature-induced changes in the liquidity of the cell membrane or its selected domains modify the structure and function of membrane proteins. Cell membrane's response to temperature variations may also be determined by its sterol content or interactions with other non-lipid organic compounds (Sung et al. 2003, Alberts et al. 2004). Temperature-induced changes in membrane properties also significantly affect water regulation in cells, and secondary water stress may occur when the rate of water uptake by the roots is slower than leaf transpiration. At temperatures below 0Â°C, liquid water changes into solid ice. Ice crystals are formed inside the protoplast which could lead to structural damage. Extracellular formation of ice may cause cell dehydration. The component processes of plant growth do not all respond to temperature in the same way. For example, in most crop species, gross photosynthesis ceases at temperatures just below 00C (minimum) and above 400C (maximum), with the highest rates being achieved in the range of 20-350C. In contrast, rates of respiration tend to be low below 200C but, owing to the thermal disruption of metabolic controls and compartmentation at higher temperatures, they rise sharply up to the compensation temperature, at which the rate of respiration equals the rate of gross photosynthesis, and there can be no net photosynthesis (Wilkinson 2000, Fitter and Hay 2002, Jenks and Hasegawa 2005, Wahid et al. 2007).
Temperature stress in plants has been broadly researched, and the problem has been widely addressed by review articles (e.g.Wang et al. 2003, Wahid et al. 2007, Jan et al. 2009), books discussing various types of stress (e.g. Wilkinson 2000, Fitter and Hay 2002, Jenks and Hasegawa 2005), studies investigating the negative effects of extreme temperatures (e.g. Iba 2002, Sung et al. 2003), etc. It should be noted that unlike homeothermic animals, plants are unable to maintain their cells and tissues at a constant optimum temperature, therefore, their metabolism, growth and development are profoundly affected by changes in environmental temperature. The above suggests that as sessile organisms, plants must be able to sense transient fluctuations as well as seasonal changes in temperature and respond to these changes by actively adjusting their biology to fit the subsequent temperature regime. Temperature is a major environmental factor that changes from season to season and undergoes daily fluctuations and short, erratic lows and highs. For this reason, the stress-inducing role of temperature is difficult to define unambiguously since the response to various temperatures is determined by the plants' ability to adapt to different climate regimes. Vegetation occurs in climate zones characterized by extreme temperatures of -50Â°C to +50Â°C, i.e. within a range of 100Â°C. The margin of thermal tolerance that conditions the stability of life processes in most plants is relatively wide, ranging from several degrees above zero to around 35Â°C, and it is genetically determined. Many genotypes specific to extreme climate conditions, from arctic to tropical, have a much wider tolerance margin. In principle, plants in the dormant state (dry germs and seed embryos, dehydrated dormant organs) are far less sensitive to temperature change, and they are able to survive through periods of extreme temperature unharmed. Metabolically active tissues have thermal activity limits which, when exceeded, lead to a reversible drop in the rate of life processes to a minimum level. Further temperature change (referred to as critical or lethal temperature) causes permanent damage to cell structures, it affects cell metabolism, impairs vital life processes and kills the protoplasm. During evaluations of plant response to extreme temperatures, special attention should be paid to the temperature of the plant which often differs from ambient temperature. In the summer, leaf temperature often exceeds ambient temperature by up to several degrees. Higher differences are noted in plants whose leaves are positioned horizontally, such as apple trees. In the spring and autumn, the night temperature of leaves, in particular when the sky is clear, may be even several degrees lower than ambient temperature. (Wilkinson 2000, Fitter and Hay 2002, Jenks and Hasegawa 2005). At a given moment, leaf temperature is determined by several factors (Tab.1). Roots demonstrate a stronger growth response to extreme temperatures than the above-ground parts of plants, and the above applies to both extreme cold and extreme heat (Fig.4). During the evolution process, roots became adapted to more stable temperatures. Nonetheless, the temperature of both the roots and other under-ground organs is also determined by factors presented in Table 1.
Plants can adapt to changes in the temperature regime through the evolution of genotypes with more appropriate morphologies, life histories, physiological and biochemical characteristics, or by plasticity. Plants also adapt to changing temperatures during the growing season by plastic responses.
2. LOW TEMPERTURE
Periodic temperature drops below zero degrees are reported on around 64% of the Earth's surface. The lowest temperatures are noted in Antarctica, reaching around -50Â°C in coastal areas and up to -90Â°C in the interior. The minimum temperature at which a given species can survive is one of the main criteria determining plant distribution on our planet. In a temperate climate, low-temperature stress eliminates or inhibits the growth and yield of valuable plants and crops (Xin and Browse, 2000, Jan et al. 2009). Plants indigenous to colder regions are usually well adapted to chilling temperatures and are, therefore, not significantly impaired by cold periods, apart from a general slowing down of the metabolic rate and growth. In a temperate climate, plants respond differently to freezing temperatures and the winter environment than other factors that occur irregularly. In the winter, chilling temperatures do not come as a surprise for plants that have adapted to the periodic, adverse vegetation factors in the course of evolution. Low temperatures are accompanied by short daytime and low radiation intensity. The adaptation to growth inhibiting factors is characteristic of the dormant state (Jan et al. 2009).
There are two types of injures a plant can sustain through exposure to low temperatures (Fig.5.) On the other hand, many plants that are native to cold climates can survive extremely low temperatures without injury (Levitt 1980).
An analysis of freezing winter temperatures as an environmental stressor should also account for the impact of other adverse factors such as low light intensity and short daytime. The above conditions arrest the growth and development of vegetation (Hopkins 2006).
The plants' ability to survive freezing and other adverse temperature changes differs from the remaining stressors. Levitt's stress avoidance theory (1980) does not apply in this case. Plants are unable to avoid freezing temperatures, and they can only protect themselves from the negative consequences of cold by increasing their tolerance to chilling. Many plants enter the dormant state to survive harsh winter weather. This is a typical feature of adaptation to freezing which is a genetically inherited trait.
Plants can be classified into three categories based on the range of lethal temperatures and the characteristics of mechanisms conditioning their resistance to low temperatures (Fig.6.)
CONSEQUENCES OF CHILLING AND FREEZING STRESS
There are two theories explaining the plants' primary response to temperature stress. The first concept, formulated by Lyons (1973), states that low temperatures induce the phase transition of cell membranes where a liquid-crystal structure is transformed into a crystal (gel) phase. Thermotropic phase changes are the primary cause of membrane dysfunctions that lead to irreversible damage and cell death. The above may produce reactive oxygen species and the accompanying oxidative stress. According to recent research, the phospholipid which initiates the phase transition of the cell membrane is phosphatidylglycerol (PG). If a PG molecule contains fatty acids with a high melting point, i.e. saturated fatty acids, then the phase transition of this lipid takes place relatively easily at low temperatures and this, in turn, induces the transformation of other phospholipids and galactolipids adjacent to PG (Los and Murata 2004, Wang, Li and Welti 2006). According to the second chilling injury theory, the primary cause of damage is the sudden increase in the concentration of free calcium ions in the cytosol (Minorsky 1989). Calcium ion concentrations increase as calcium channels in the plasmalemma become opened due to sudden depolarization (e.g. Lecourieux, Ranjeva and Pugin 2006). In chilling-sensitive plants, calcium opens the stomata, and transpiration significantly exceeds water uptake by the roots (Liang, Wang and Ai 2009). In many sensitive species, the first indication of cold stress is striking wilting of the leaves, despite optimal water supply in the soil (Mahajan, and Tuteja 2005, Solanke and Sharma 2008). The release of calcium ions into the cytosol has many secondary effects, including induced gene expression which could result from changes in the content or distribution of cell hormones, mainly ABA. This phenomenon is in particularly related to the acidification of the cytoplasm at low temperatures (and the corresponding alkalization of the vacuoles) which, at least in part, is actively controlled by H+-transport from the cytoplasm to the vacuole catalyzed by H+-ATPase located on the vacuolar membrane. The inactivation of this enzyme has been reported to occur much earlier than other symptoms of cell injury (Yoshida et al. 1999, Lindberg, Banas, and Stymne 2005). Chilling affects the entire internal environment of each cell and each molecule within the cells (Kratsch and Wise 2000). The rate and extent of injury is determined by temperature, its duration as well as the chilling rate. Sudden temperature drops (thermal shock) have particularly damaging consequences. The lower the temperature and the longer its effect, the greater the extent of the sustained injury(Mahajan and Tuteja 2005, Solanke and Sharma 2008). Plant structures and physiological cell processes have varied sensitivity to chilling temperatures (Fig. 7). Most injuries are sustained in the cell membrane which may represent a potential site of perception and/or injury (Lindberg, Banas, and Stymne 2005). There are changes in the viscosity and liquidity of the membrane, leading to an increase in diffusion resistance and, in many cases, enzyme inactivation. The reversibility of those effects is determined by the severity of damage. Changes in chemical composition may be observed as the result of lipid degradation, the release of fatty acids and changes in the activity of metabolizing enzymes, peroxidation, disintegration of lipid-protein bonds and higher membrane permeability. The chemical composition of the cytoplasm and differences in lipid quality in various chilling-sensitive species determine the phase transition point, i.e. the point at which the membrane is transformed from a liquid-crystal state into a gel state (Solanke and Sharma 2008, Jan et al. 2009). This change in the membrane's physical state impairs its normal functioning. In most chilling-sensitive plants, the phase transition point is around 10Â°C. Chilling sensitivity is mostly related to a higher content of saturated fatty acid residues in lipids, while the cold-hardiness mechanism is explained by the desaturation of fatty acids which enables the plant to quickly acclimatize to low temperatures. The above is only one of the factors explaining variations in the plants' response to temperature stress (Lindberg, Banas, and Stymne 2005, Zhang and Tian 2010). Interactions between membrane components, including lipid-lipid and lipid-protein, are also believed to play an important role. Higher sterol concentrations increase membrane rigidity. The role of membrane proteins during chilling is also a source of controversy, but there is general agreement that conformational changes in protein-lipid systems may lead to membrane disintegration and dysfunction (Los and Murata 2004, Lindberg, Banas, and Stymne 2005). Frost-induced changes may lead to inhibited protoplast movement, excessive protoplast vacuolization, damage to the endoplasmic reticulum, drop in turgidity and higher membrane permeability. Cytoplasmic streaming and photosynthesis, including thylakoid functioning in chloroplasts (as demonstrated by enhanced in vivo chlorophyll fluorescence), are most susceptible to reversible disruptions. Irreversible damage, including injuries caused by stressors other than temperature, is also most likely to affect thylakoid membranes, mostly photosystem II. Chloroplast lipids undergo various metabolic changes in both chilling-sensitive and cold-hardy plants. Higher levels of galactolipase activity and, consequently, higher free fatty acid concentrations are noted in the chloroplasts of chilling-sensitive species (faba beans, beans, tomatoes, maize) than in cold-hardy plants (spinach, pea). Lower temperatures disrupt the maintenance of the proton gradient in thylakoid membranes conditioning ATP synthesis. Powerful radiation during or directly after chilling intensifies the relevant injuries and retards, or even disables, damage repair in both chilling-sensitive and cold-hardy plants. Long-term frost inhibits the synthesis of chlorophyll and starch (Muller, Hikosaka and Hirose 2005, Liang, Wang, and Ai 2009, Sun et al. 2010). Other membranes (plasmalemma and tonoplast) are damaged after relatively longer exposure, as demonstrated by membrane cells' ability to plasmolyze and vital staining. Those injuries are irreversible. Other metabolic functions are marked by varied sensitivity to low temperatures which cause metabolic disorders and lead to toxin accumulation, e.g. respiration efficiency may be higher or lower subject to environmental factors that accompany freezing temperatures. Chilling may also inhibit the activity of many oxidoreductive enzymes, such as catalase, leading to the accumulation of hydrogen peroxide and the production of free radicals (Suzuki and Mittler 2006, Liang, Wang, and Ai 2009, Sun et al. 2010). In sublethal cold stress, fruit ripening and seed germination are most severely inhibited (e.g. Kumar and Bhatla 2006).
Frost leads to the appearance of stress which is linked not directly to low temperature, but to freezing (crystallization) of water in the plant (Mahajan and Tuteja 2005). Intracellular and extracellular crystallization produces different effects. Ice crystals are formed readily in those parts of the plant where temperature drops most rapidly and where water freezes most easily (due to high water potential), mostly vascular bundles and intracellular spaces in above-ground parts where water vapor undergoes condensation. Ice crystals spread quickly via vessels and other tissues with uniform structure. The presence of air-filled intercellular spaces as well as tissues with lignified or cutinized walls slows down crystallization. Ice formation is accelerated by ice-nucleation active bacteria of the genera Ervinia and Pseudomonas. The proteins formed on the outer bacterial cell wall react with water particles and facilitate the formation of ice crystals at temperatures just below 0Â°C. In the absence of ice-nucleation active bacteria on the surface of tissues and on the walls of intracellular spaces, ice formation would begin at temperatures several degrees lower due to the supercooling of water solutions.
If tissue is supercooled rapidly (e.g. faster than 5 K min-1) and the cells have high water potential, or if cell water had been first deeply supercooled, ice may be formed in the protoplast. The above invariably leads to cytoplasm destruction and cell death (Fitter and Hay 2002, Rajashekar 2000, Jan et al. 2009, Janska et al. 2010). Water freezing in intracellular spaces is a less dangerous phenomenon. In nature, where temperature decline is generally slow (1 to 5 K min-1), crystallization usually takes place outside the protoplast in intracellular spaces and between the cell wall and the protoplast (partly due to the extracellular fluid having a higher freezing point, i.e. lower solute concentration, than intracellular fluid). The above leads to extracellular crystallization. Vapor pressure decreases in the spaces above ice, and a water potential gradient is created between the unfrozen interior of the cell and the extracellular environment. Water moves along this gradient into extracellular spaces where it is crystallized (Fitter and Hay 2002, Jan et al. 2009, Janska et al. 2010). Cells are dehydrated (secondary stress) and they contract due to desiccation. The lower the surrounding temperature, the longer it takes for an equilibrium to be reached between the water potential above ice and inside cells, and the greater the effect of cell dehydration (Solanke and Sharma 2008).
Multiple forms of membrane damage can occur as a consequence of freeze-induced cellular dehydration including expansion-induced-lysis, lamellar-to-hexagonal-II chase transitions and fracture jump lesions. The above leads to cell contraction and the associated changes in reactions between the plasmalemma and the cell wall, partial loss of plasmalemma due to exocytosis and endocytosis, changes in the structure of the plasmalemma and other cell membranes, and the creation of protein-deprived lipid areas in the membrane. The greatest damage is done to the plasmalemma. Dehydration also increases the concentration of solutions in the cytosol and the cell sap, leading to higher salinity (Mahajan and Tuteja 2005, Solanke and Sharma 2008, Jan et al. 2009). Conformational changes in proteins found in the plasmalemma and other membranes lead to changes in the activity of various membrane enzymes, including ATPases responsible for the movement of protons and other ions through membranes (Lindberg, Banas, and Stymne 2005). Some ions, accumulated in cells by ion transporters (e.g. potassium ions), are diffused after thawing into intracellular spaces together with water, e.g. in leaf tissue. Certain proteins, such as the thylakoid coupling factor, become dissociated in the process. The effect of chill injury on life processes is often visible when plants resume their normal growth after freezing temperatures subside. Even partial degradation of thylakoid membranes inhibits photosynthesis, and the process may be reversible. PS II activity may be partially or completely inhibited, and the balance between the light-dependent phase and CO2 assimilation may be upset. There is a rise in photorespiration intensity (Alam, Nair, and Jacob 2005) . Changes in the mitochondria and the respiration process are not as profound. In strongly dehydrated cells, the membrane undergoes lyotropic phase transitions, and hexagonal arrangements are formed in lipid bilayers of a single membrane or two layers of two adjoining membranes (e.g. plasmalemma and endoplasmic reticulum). The membranes' primary structure is not always restored after thawing, and water is diffused into the extracellular environment together with ions through membrane channels. Cell dehydration caused by extracellular crystallization increases the concentrations of salt and organic acids in the protoplast which, in turn, may lead to protein denaturation and enzyme inactivation (Mahajan and Tuteja 2005, Solanke and Sharma 2008). Few enzymes remain active at below zero temperatures, but some of them are activated, such as phospholipase D which catalyzes the hydrolysis of phospholipids (Ruelland et al. 2002). The degradation of membrane lipids begins during freezing and after thawing, releasing unsaturated fatty acids which are peroxidized. Chlorophyll may be also be photooxidized in green tissues exposed to light (Sung et al. 2003). Chill injuries may occur not only during freezing, but also during the thawing of tissue. Plant survival is also determined by post-thawing environmental factors - rapid temperature growth and high light intensity may disturb metabolic pathways in cells and cause additional damage. During rapid melting of ice, the cell is rehydrated, and it quickly increases its volume. The above leads to tension and cracks in cell structures, mostly in the cytoplasm which is the site of primary cell injury. The above changes have less damaging consequences for dormant plants. In a temperate climate, winter frost is not a typical stressor for plants, but freezing temperatures could be a source of stress if they occurred in the spring or summer (Muller, Hikosaka and Hirose 2005).