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Resistance is related to frost tolerance, i.e. the ability of the organism to survive low temperatures without damage. In regions characterized by seasonal climate change, plants' resistance to freezing fluctuates periodically - it is the lowest during intensive elongation growth in the spring, and it rises significantly in the fall when growth is arrested by the direct effect of low temperature or the combined effect of shorter daytime and temperature drop (Li et al. 2005). Frost resistance is usually achieved by preventing ice formation in the symplast. An important mechanism preventing or delaying symplastic ice formation is frost plasmolysis. Poorly-hydrated plants which are acclimatized to water stress usually show increased cold resistance, e.g. plants which are extremely tolerant to drying out, e.g. embryos of ripened seeds, can be conserved alive at -2000C without damage (Jan et al. 2009). Species-specific cold resistance is a genetically programmed trait that can be modified by both endogenous and exogenous factors. For a vast number of species, frost tolerance is not a static feature, but it is closely correlated with season, it fluctuates in various growing periods, and it is not identical for all organs (Rorat et al. 2006, Hekneby, Antolin, and Sanchez-Diaz 2006). The above-ground parts of wheat seedlings were acclimatized even to -20Â°C, but the roots' sensitivity to frost did not change. Acclimatization can be accelerated by hardening the plants, i.e. exposing them to increasingly lower temperatures on successive days, initially above zero, followed by insignificantly below zero (Li, Wu and Liu 2005, Zhang and Tian 2010). This process is continued for several weeks. Plants are characterized by the greatest frost resistance one to three weeks from the beginning of exposure to freezing temperatures. The period of deacclimatization, i.e. dehardening, is much shorter, and it usually lasts several days. The higher the ambient temperature, the faster the deacclimatization process. After dehardening, repeated exposure to frost can severely damage many plants (Li, Junttila and Palva 2004, Burbulis, Kupriene, and Blinstrubiene 2008).
Plant organs are also marked by varied sensitivity to frost (Li, Wu and Liu 2005, Rorat et al. 2006). Roots are most susceptible to the damaging effects of freezing temperatures, shoots are less sensitive, while tree trunks and older branches are characterized by the highest frost resistance (Muller, Hikosaka and Hirose 2005, Kato-Noguchi 2007). Snow cover minimizes the temperature drop in the soil, and it protects crops from freezing. The cold sensitivity of flowers is determined by the given species' phenological growth stages (Thakur et al. 2009, Ohnishi, Miyoshi, and Shirai 2010)
Abscisic acid stimulates and speeds up plant hardening. According to Weiser (1970), acclimatization, and perhaps also hardening, are determined by modifications in gene expression. In this case, ABA can enhance cold resistance if it is able to induce the expression of the respective genes (Gusta, Trischuk, and Weiser 2005). Gibberellins and auxins deliver an opposite effect. Substances that retard gibberellin synthesis accelerate hardening. Intensive nitrogen fertilization generally delays dormancy and increases susceptibility to freezing. Heavy potassium fertilization has the opposite effect by increasing the frost resistance of both herbaceous and arborescent plants. The concentrations of sugar and other osmoprotectors that protect the cell from dehydration increases in the cytosol and vacuoles (Liang, Wang and Ai 2009).
Fluid supercooling inside the cell is yet another factor that increases the plants' cold resistance by delaying crystallization in the cell. The presence of substances dissolved in the vacuolar sap lowers crystallization temperature. In small, weakly vacuolated cells, water may undergo deep supercooling. In large and hydrated parenchymal cells and xylem vessels, the supercooled state is very unstable, and it rarely lasts longer than several hours. Supercooling provides temporary protection against freezing caused by, for example, strong ground frost. In tissues comprising small, densely packed and weakly vacuolated cells whose walls prevent ice crystals from spreading, a supercooled state may persist until the temperature drops below a threshold value. The accumulation of non-polar lipids on the surface of the plasmalemma also prevents ice penetration from the apoplast to the cell interior. In herbaceous plants, the supercooling of water is observed at -1 to -150C, and in arborescent plants at -30Â°C, and even -50Â°C. Such a high degree of supercooling is observed only in some living tissues, such as core parenchymal cells, meristematic tissue, leaf bud scales and flower buds. When ambient temperature drops below the critical supercooling point, this meta-stable state is rapidly disrupted, and ice is formed inside the cells, ultimately leading to their death. In some extremely frost-resistant tree species, the protoplasm is able to vitrify. Vitrification is stimulated by a high concentration of sucrose and other sugars. In this relatively stable condition, it is possible to cool cells almost to absolute zero without destruction (Rajashekar 2000, Hopkins 2006, Jan et al. 2009).
Membranes are restructured under exposure to cold before the temperature drops below zero. In these conditions, the water potential is gradually lowered with a simultaneous drop in the osmotic potential due to the accumulation of carbohydrates in vacuoles. ABA is accumulated, and it induces the synthesis of specific proteins. The next stage brings intensified changes in the cell membrane - degradation of phosphatidylcholine and phosphoinositol, accompanied by a continued increase in ABA levels and protein synthesis modifications (Gusta, Trischuk, and Weiser 2005, Lindberg, Banas, and Stymne 2005). Cryoprotectants, substances that directly protect the membrane from damage, are also synthesized at this stage. Rigid membranes are less likely to be deformed during frost-induced dehydration, and they protect cells against freezing more effectively. This parameter is largely dependent on the sterol content of cells (Hopkins 2006, Janska et al. 2010).
In addition to membrane unsaturation, it appears that lipid asymmetry in the membrane also contributes to the physical structure of the membrane at low temperature (Gomes et al.2000).
The mechanism protecting chloroplast membranes enables the plant to begin photosynthesis as soon as ambient temperature increases.
The cold resistance of plants is also determined by the following mechanisms:
1. Thermal insulation which delays and minimizes heat loss, e.g. shoot apices are often covered with dense foliage (rosette plant habit) or they winter under a layer of leaves or litter (geophytes). Frost tender organs are often rejected before the onset of very low temperatures (deciduous plants shed leaves in the fall). In high mountainous regions of tropical zones, the leaves of large rosette plants close above the tip at night to protect the interior from freezing (Hopkins 2006) .
Water freezing in intertissue spaces, e.g. between the seed coat and the embryo or between bud scales, where extensive areas are covered with ice.
Cell structures are protected against excessive dehydration with an accompanying increase in the effectiveness of barriers that prevent ice crystals from propagating from the apoplast inside the cell. The following mechanisms are involved:
osmotic pressure increases to keep water inside the cell, and the water potential decreases due to the accumulation of osmotically active compounds (simple sugars and oligosaccharides, polyols, low-molecular-weight nitrogen compounds, such as selected amino acids) in vacuoles and hydrophilic proteins in the cytoplasm (Rorat 2006, Liang, Wang and Ai 2009). The share of highly polar lipids in the membrane structure increases, such as phosphatidylcholine and phosphatidylethanolamine in the plasmalemma and cytoplasmic membranes or digalactosyldiacylglycerol in chloroplast membranes, which increases matrix interactions inside the cell.
the membrane is enriched with more stable lipids containing polyunsaturated fatty acid residues, selected sterols and cryoprotectants are accumulated in the cytoplasm to protect cell structures against strong dehydration (Lindberg, Banas, and Stymne 2005, Zhang and Tian 2010). These substances stabilize membrane structure and prevent conformational protein changes. They counteract the accumulation of salt ions and selected organic acids in the cell, and they protect proteins against denaturation. Small proteins, whose synthesis is enhanced or induced under exposure to low temperatures, play a protective role. Some of them show significant homology to proteins synthesized in response to water stress, e.g. to dehydrin (Rorat et al. 2006). The cell wall plays an important role in protecting the cell against the adverse consequences of dehydration, and it is the main barrier to ice penetration.
In addition to mechanisms responsible for resistance to the primary consequences of frost, cold resistant plants develop acclimatization mechanisms that enable them to avoid secondary thermal stress at below zero temperatures, such as photoinhibition, draught, oxygen deficiency (under ice cover) or mechanical effects of ice load (e.g. Alcázar et al. 2011).
3. HIGH TEMPERATURE
Heat stress occurs when a rise in temperature has negative consequences for a plant. It is a complex function of intensity (temperature in degrees), duration and the rate of temperature increase. For plants inhabiting very cold climates such as the Arctic, temperatures in the region of 15Â°C can already be a source of heat stress. In a temperate climate, heat stress takes place in the temperature range of 35 to 40Â°C. In scientific literature, heat stress denotes temperatures that exceed the optimum values by around 10-15Â°C (e.g. Larkindale et al. 2005). Plants can be divided into three groups, subject to their sensitivity to high temperature (Fig. 8). In geographic zones with a hot climate, in habitats marked by high fluctuations in daily temperature (soil surface, littoral zone, shallow waters) or seasonal fluctuations and in volcanic areas, temperature levels can be lethal for vascular land plants. High absorption of solar energy during windless weather can increase the temperature inside plant tissues in excess of the ambient temperature. Creeping grass shoots, the runners and tillers of young plants can also be subjected to heat stress. The lethal temperature range (thermal death point) is determined by the duration of tissue exposure to high temperature (Tab.2). Only single-celled organisms can complete their life cycle during continued exposure to temperatures higher than 500C, while only prokaryotic organisms can survive in temperatures higher than 600C.
CONSEQUENCES OF HEAT EXPOSURE
At very high temperatures, severe cellular injury and even death may occur within minutes or even seconds (due to denaturation and/or aggregation of proteins), while at moderately high temperatures, injures or death may occur only after long-term exposure (due to disruptions in basic metabolic processes). The adverse effects of overheating are directly noticeable. The morphological symptoms of heat stress include scorching of leaves and twigs, sunburns on leaves, branches and stems, leaf senescence and abscission, shoot and root growth inhibition, fruit discoloration and damage, and reduced yield. Cell size reduction, closure of stomata and curtailed water loss is observed at the tissue and cellular level. At the sub-cellular level, major modifications occur in chloroplasts (changing the structural organization of thylakoids, loss of grana stacking or its swelling) (Wahid et al. 2007; Mitra and Bhatia 2008). In vascular land plants, the negative consequences of elevated temperature are often related to secondary stress, namely a negative water balance (leading to the perturbation of many physiological processes) due to intensive leaf transpiration during daytime. Under field conditions, high temperature stress is frequently associated with reduced water availability (higher during daytime than at night). Heat stress may secondarily induce oxidative stress via the generation and the reactions of activated oxygen species (Xu et al., 2006, Almeselmani et al. 2006).
Metabolic pathways and processes show varied sensitivity to temperature which may result in a deficit or an excess of selected metabolites. It is generally believed that the processes taking place in membranes are most sensitive to temperature change. A heat-induced increase in membrane liquidity (either by denaturation of proteins or an increase in unsaturated fatty acids) and changes in reactions between lipid and protein components impair membrane functions (Savchenko et al. 2002, Whaid et al. 2007), including the functioning of ion and water channels, ion transporters, metabolite transport, energy generation and other processes. Ion leakage from the cell is observed, photosynthesis and respiration are also impaired (Whaid et al. 2007; Wang et al. 2009). It has also been suggested that changing membrane fluidity plays a central role in sensing (plant thermometer) and influencing gene expression both under high and low temperatures (Plieth, 1999). Photochemical reactions in thylakoid lamellae and carbon metabolism in the stroma of chloroplast have been suggested as the primary sites of injury at high temperatures (Yang et al. 2006, Wang et al. 2009). Thylakoid membranes are particularly sensitive to high temperature, and this especially applies to photosystem II whose activity is greatly reduced or even partially stopped under high temperatures (Salvucci and Crafts-Brandner 2004, Camejo et al. 2005; Marchand et al. 2005). High temperature has a greater influence on the photosynthetic capacity of C3 plants than C4 plants (Crafts-Brandner and Salvucci 2002). Heat shock reduces the amount of photosynthetic pigments (Wang et al. 2009), soluble proteins, rubisco binding proteins (RBP), large-subunits (LS) and small-subunits (SS) of rubisco in darkness but increases them in light (Kepova et al. 2005). Moreover, heat stress greatly affects starch and sucrose synthesis, as demonstrated by the reduced activity of sucrose phosphate synthase, ADP-glucose pyrophosphorylase and invertase (Wahid et al. 2007, Sumesh et al. 2008). In any plant species, the ability to sustain leaf gas exchange under heat stress is directly correlated with heat tolerance. During the vegetative stage, high daytime temperature can cause damage to compensated leaf photosynthesis, reducing CO2 assimilation rates (Crafts-Brander and Salvucci, 2002; Morales et al., 2003). Photosynthesis is more sensitive to heat than dark respiration which could have additional consequences under prolonged stress, including the depletion of carbohydrate reserves and plant starvation (Sumesh et al. 2008). Heat stress rapidly increases selected phytohormone levels, including abscisic acid (ABA), ethylene and salicylic acid, and it decreases cytokinin and gibberellin concentrations (Dat et al. 2000, Talanova et al. 2003, Larkindale and Huang 2004). The overlapping effects of the above changes in hormone levels speed up plant ageing.
MECHANISM OF PLANT RESISTANCE TO HIGH TEMPERATURE
Plants rely on two adaptation mechanisms to survive high temperatures: the ability to prevent excessive temperature growth in tissues or alleviate its effects and the heat tolerance of the protoplasm.
Survival in hot, dry environments can be achieved in a variety of ways, by combinations of adaptations (Fitter and Hay 2002). Plants growing in a hot climate avoid heat stress by reducing the absorption of solar radiation. This ability is supported by the presence of small hairs (tomentose) that form a thick coat on the surface of the leaf as well as cuticles, protective waxy covering. In such plants, leaf blades often turn away from light and orient themselves parallel to sun rays (paraheliotropism). Solar radiation may also be reduced by rolling leaf blades. Plants with small leaves are also more likely to avoid heat stress: they evacuate heat to ambient more quickly due to smaller resistance of the air boundary layer in comparison with large leaves. Plants rely on the same anatomical and physiological adaptive mechanisms that are deployed in a water deficit to limit transpiration. In well hydrated plants, intensive transpiration prevents leaves from heat stress, and leaf temperature may be 6 K or even 10-15 K lower than ambient temperature. Many species have evolved life histories which permit them to avoid the hottest period of the year. This can be achieved by leaf abscission, leaving heat-resistant buds, or in desert annuals, by completing the entire reproductive cycle during the cooler months (Fitter and Hay 2002). Such morphological and phonological adaptations are commonly associated with biochemical adaptations favoring net photosynthesis at high temperatures (in particular C4 and CAM photosynthetic pathways), although C3 plants are common in desert floras (Fitter and Hay 2002).
Heat tolerance is generally defined as the ability of the plant to grow and produce economic yield under high temperatures. This is a highly specific trait, and closely related species, even different organs and tissues of the same plant, may vary significantly in this respect. The above is affected by climate conditions and the species' geographic origin. Plants native to cold regions (tundra, high mountain ranges) are much more sensitive to heat than temperate flora. The latter, in turn, are more susceptible to high temperatures than desert and tropical plants. The highest heat tolerance is demonstrated by selected sedge and grass species, mainly C4 plants. Heat tolerance is associated with greater enzyme thermostability and a higher share of saturated fatty acids in membrane lipids which increases the lipid phase transition (melting) temperature and prevents a heat-induced increase in the membrane's liquidity. It is believed that phosphatidylglycerol is the phospholipid initiating phase transitions in thylakoid membranes. Heat tolerance leads to a rapid genome reaction even during short-term overheating. The biosynthesis of heat stress proteins (HSP) which prevent macroparticle denaturation is induced (Kotak et al. 2007; Al-Whaibi 2010). During exposure to high temperature, plants synthesize two groups of heat stress proteins: four high-molecular weight HSPs (HSP 100, HSP 90, HSP 70, HSP 60) and several low-molecular weight HSPs (smHSPs). Those proteins remain stable over a certain period of time, and they are probably the main factor enabling plants to survive a temperature increase. HSPs are found in the cytoplasm and organelles such as the nucleus, mitochondria, chloroplasts and endoplasmic reticulum. The tolerance conferred by HSPs results in improved physiological phenomena such as photosynthesis, assimilate partitioning, water and nutrient use efficiency, and membrane stability. Those improvements make plant growth and development possible under heat stress (Wang et al. 2004). The HSPs/chaperones may be involved in stress signal transduction, gene activation and the regulation of the cellular redox state. They also interact with other stress-response mechanisms such as the production of osmolytes and antioxidants (Kotak et al. 2007; Wahid et al. 2007; Al-Whaibi 2010). In heat-stressed plants, the induction of HSP synthesis inhibits the biosynthesis of other proteins. A plant's resistance to heat is determined by protein synthesis in cells that are lost with age. For this reason, ageing organs (and organisms) have impaired ability to acclimatize to high temperature. Smaller quantities of HSPs are also determined at optimal temperature, but in this environment, they play a different role than during and after stress. Under optimal conditions, HSPs regulate the formation of protein structures from newly emerged polypeptide strings to protect the cell from proteins that are non-functional due to synthesis "errors". At excessively high temperatures, HSPs minimize cell injuries by protecting cell proteins from denaturation and creating chelate bonds with ions leaking from the vacuoles into the cytosol (Kotak et al. 2007; Wahid et al. 2007; Al-Whaibi 2010). An increased content of abscisic acid (ABA) mediates the acclimation/adaptation of plants to desiccation by modulating the up- or down-regulation of numerous genes (Talanova et al. 2003; Wahid et al. 2007). It is suggested that the induction of several HSPs (e.g., HSP70) is regulated by ABA (Snyman and Cronje 2008). Increased ethylene secretion at high temperatures leads to the abscission of reproductive organs; this is accompanied by both reduced levels and transport capacity of auxins to reproductive organs (Wahid et al. 2007). Among other hormones, salicylic acid (SA) has been suggested to be an important component of signaling pathways in response to systemic acquired resistance (SAR) and the hypersensitive response (HR) during heat-stress (Kawano et al., 1998, Wang and Li 2006). Gibberellins and cytokinins have an opposite effect on high temperature tolerance than ABA. The potential roles of other phytohormones in plant thermotolerance are yet unknown (Wahid et al. 2007). Under stress, different plant species may accumulate a variety of osmolytes such as sugars and sugar alcohols (polyols), proline, tertiary and quaternary ammonium compounds, and tertiary sulphonium compounds (Singh and Grover 2008). The accumulation of such solutes may contribute to enhanced stress tolerance of plants, e.g. proline and glycinebetaine may buffer the cellular redox potential under heat and other environmental stresses (Wahid and Close, 2007); gama-4-aminobutyric acid (GABA) has a physiological role in the mitigation of stress effects (Kinnersley and Turano, 2000). High-temperature stress induces the production of phenolic compounds such as flavonoids and phenylpropanoids. The heat-induced increase in the activity of phenylalanine ammonia-lyase (PAL) is considered to be the cell's main acclamatory response to heat stress (Wahid and Ghazanfar, 2006; Wahid, 2007). Carotenoids of the xanthophylls family and selected terpenoids, such as isoprene or tocopherol, stabilize and photoprotect the lipid phase of thylakoid membranes during exposure to strong light and/or elevated temperatures (Wahid and Ghazanfar, 2006; Wahid, 2007). The expression of stress proteins is an important adaptive mechanism for environmental stress tolerance. Most stress proteins are soluble in water and, therefore, they contribute to stress tolerance, presumably by hydrating cellular structures (Wahid and Close, 2007). Heat stress also induces the synthesis of other plant proteins, including ubiquitin (Sun and Callis, 1997), cytosolic and chloraplasts Cu/Zn-SOD (Tang et al. 2006) and Mn-POD (Brown, Li and Ic 1993), cytosolic (Iba K. 2002) and chloraplasts APX (Tang et al. 2006), and other antioxidant enzymes (Sairam et al. 2000; Almeselmani et al. 2006), protenins of late embryogenesis abundant (LEA) (Goyal, Walton, and Tunnacliffe 2005) and dehydrins. Their main function is to protect cellular and sub-cellular structures against oxidative damage and dehydrative forces.
ADAPTATION TO HIGH TEMPERATURE
Plants adapt to heat already after several hours of exposure to a temperature that evokes a stress response, but remains below the lethal temperature level (Xu et al. 2006). For most land plants, heat stress is triggered at temperatures slightly above 35Â°C, and in grasses - at 38-40Â°C. The loss of resistance (dehardening) is a slower process that lasts several days in optimal growth conditions (Sung et al. 2003, Burke and Chen, 2006). During acclimatization, the structure of the cell membrane changes by increasing the share of saturated fatty acids in the lipid layer. More unsaturated acyl residues are removed from the sn-2 position in a glycerolipid molecule by the respective hydrolases. They are replaced with saturated fatty acid residues (mostly 18-carbon chains) with the involvement of the respective acetyltransferases and lipid transport proteins. At the current state of knowledge, it remains unknown whether a higher or a lower degree of membrane lipid saturation is beneficial for high-temperature tolerance (Klueva et al. 2001, Rahman et al. 2004). It is believed that the synthesis of heat stress proteins is also an effective mechanism protecting the plant from high temperature and other HSP synthesis-inducing stressors. In many plants, heat tolerance varies on a seasonal basis in view of their growth cycle and changes in seasonal temperature (e.g. Froux et al. 2004). During active growth, all plants are highly sensitive to temperature stress. Selected species of land plants increase their resistance to heat only in the summer, while others demonstrate the highest level of tolerance during winter dormancy. Dormant plants become resistant to stress upon reaching a developmental stage induced by factors other than high environmental temperature. In many land plant species, noticeable changes in heat tolerance are not observed. Due to the close correlation between drought and high temperature, the effects of each stressor on field-grown plants can be difficult to distinguish, and adaptations to arid environments can be effective only if they lead to avoidance or tolerance of both stresses (Fitter and Hay 2002).