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Physiological basis of cold tolerance

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Cold tolerance is the result of complex physiological mechanisms involving many cell and plant traits. Plants differ in their tolerance to chilling (0-15 ºC) and freezing (< 0ºC) temperatures. Different studies have indicated that the membrane systems of the cell are the primary site of freezing injury in plants (Levit 1980, Steponkus 1984). In addition, it is well established that freeze-induced membrane damage results primarily from the severe dehydration associated with freezing (Steponkus 1984, Steponkus et al. 1993).

Many species of tropical or subtropical origin are injured by non-freezing low temperatures and exhibit various symptoms of chilling injury such as chlorosis, necrosis, or growth retardation. In contrast, chilling tolerant species are able to grow at such cold temperatures. Membrane damage is the primary consequence of cold injury. Multiple forms of membrane damage can occur as a consequence of freeze-induced cellular dehydration including expansion-induced-lysis, lamellar-to-hexagonal-II phase transitions, and fracture jump lesions (Steponkus et al. 1993).

Cold acclimation by plants is to stabilize the membranes against freezing injury preventing expansion-induced-lyses and the formation of hexagonal II phase lipids. This ability to adapt has an impact on the distribution and survival of the plant and on crop yields. Multiple mechanisms appear to be involved in this stabilization process. The well-characterized one is the changes in lipid composition (Steponkus et al. 1993).

Secondly, temperature induced change in membrane fluidity is another consequences in plants during low-temperature stresses and might represent a potential site of perception and/or injury (Horvath et al. 1998, Orvar et al. 2000). Adaptation of living cells to chilling temperatures is a function of alteration in the membrane lipid composition by increased fatty acid unsaturation.

Genetically engineered tobacco plants over-expressing chloroplast glycerol-3-phosphate acyltransferase (GPAT) gene (involved in phosphatidylglycerol fatty acid desaturation) from squash (Cucurbita maxima) and A. Thaliana showed an increase in the number of unsaturated fatty acids and a corresponding decrease in the chilling sensitivity. At low temperature, greater membrane lipid unsaturation appears to be crucial for optimum membrane function.

An Arabidopsis fatty acid biosynthesis (FAB1) mutant with more saturated membranes showed a decreased quantum efficiency of photosystem II (PSII), chlorophyll content and the amount of chloroplast glycerolipids after prolonged exposure to low temperature (Wu et al. 1997). A triple mutant fatty acid desaturation (fad3-2 fad7-2 fad8) devoid of trienoic fatty acids (18:3 or 16:3) produced a phenotype similar to FAB1, when plants were subjected to prolonged low-temperature exposure (Routaboul 2000).

Similarly, fad5 and fad6 mutants with more saturated membranes became chlorotic and showed growth retardation during low-temperature incubation (Hugly et al. 1992). In addition to membrane unsaturation, it appears that lipid asymmetry in the membrane also contributes to membrane physical structure at low temperature (Gomes et al. 2000) The accumulation of sucrose and other simple sugars that typically occurs with cold acclimation also seems likely to contribute to the stabilization of membranes as these molecules can protect membranes against freeze-induced damage in vitro (Strauss et al. 1986, Anchordoguy et al. 1987).

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GradesFixer. (2019). Physiological basis of cold tolerance. Retrived from https://gradesfixer.com/free-essay-examples/physiological-basis-of-cold-tolerance/
GradesFixer. "Physiological basis of cold tolerance." GradesFixer, 28 Jan. 2019, https://gradesfixer.com/free-essay-examples/physiological-basis-of-cold-tolerance/
GradesFixer, 2019. Physiological basis of cold tolerance. [online] Available at: <https://gradesfixer.com/free-essay-examples/physiological-basis-of-cold-tolerance/> [Accessed 6 August 2020].
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