Cold tolerance

The tubers start to become freeze tolerant (LD50 at -5°C) toward the end of October, prior to leaf senescence (Ishikawa and Yoshida, 1985). Tolerance increases to -11°C by mid-December. Increased low temperature tolerance did not appear to be due to changes in tuber moisture content the role of inulin depolymerization in increased cold tolerance has not been assessed. 

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Vineyard site is important to wine quaUty and character and interacts with variety. The general climate must not be too cold, too hot, or too humid. A mild, dry climate that still induces a dormant season, like the Mediterranean area and California, is desirable. A relatively constant weather pattern year-to-year is also sought. The nearer to the limits of cold tolerance, for example, that the climate comes, the more likely are disastrous vintages. The modifying influence of close bodies of water, sun-facing slopes, or frost-resisting air drainage can make one vineyard more desirable than another nearby. 

Duncan, D.R. Widholm, J.M. (1987). Proline accumulation and its implication in cold tolerance of regenerable maize callus. Plant Physiology, 83, 703-8. 

Wharton DA, Surrey MR. Cold tolerance mechanisms of the infective larvae of the insect parasitic nematode. Heterorhabditis zelandica, Poinar, Cryo Letters. 1994 15 353-360. 

The temperature effect on the decay rate of H202 in unfiltered Sharpes Bay water was determined by allowing samples to equilibrate at several temperatures (Figure 6). H202 was spiked in all samples, and the decay was followed for several half-lives. With lower water temperatures the decay rate constants were lower. As yet this has not been verified over a season. As water temperatures change the relationship may differ for cold-tolerant species. H202 decay studies have also been conducted in waters from the... 

A partial list of physiological functions til at have been determined to be affected by vitamin C deficiencies includes (1) absorption of iron (2) cold tolerance, maintenance of adrenal cortex (3) antioxidant (4) metabolism of tryptophan, phenylalanine, and tyrosine (5) body growth (6) wound healing (7) synthesis of polysaccharides and collagen (8) formation of cartilage, dentine, bone, and teeth and (9) maintenance of capillaries. 

The subject of this chapter will be to summarise the biochemical and molecular changes which take place during the process of cold acclimation and the acquisition of freezing stress tolerance. We will discuss how polypeptides correlated with the acclimation process might play a role in increased cold tolerance and we will focus on recent results emerging from molecular studies. For further treatment of the subject the reader is referred to a number of recent review articles (Steponkus, 1984 Guy, 1990 Thomashow, 1990). The biochemistry and physiology of cold acclimation is described in detail by Levitt (1980). 

As a consequence of modifications in enzyme activities several soluble components can change their levels during the cold response. For instance an increase or decrease of components like soluble carbohydrates, proline and polyamines has been correlated with the acquisition of cold tolerance. 

The co-identity of different proteins can be confirmed only by comparisons of amino acid sequences or by immunological cross-reactions. That cold-regulated polypeptides have a role in the acquisition of cold tolerance is supported by the general observation that the appearance of most proteins is temporally correlated with the onset of freezing tolerance. The polypeptides are detected as long as the plants are kept at low temperatures but decline when the temperature is raised as, for example, demonstrated by Guy Haskell (1987, 1988) for spinach. Similar associations of appearance and decline of polypeptides have been reported for alfalfa (Mohapatra et al., 1987a,b). 

Analysis of changes in in-vivo- and m-v/tro-synthesised proteins is a very descriptive approach to understanding the phenomenon of cold acclimation and cold tolerance. For a functional analysis a molecular dissection of the process is required. This will allow investigators to determine the level (transcriptional/translational) at which the appearance of the new mRNAs is regulated, and the sequence information of the cold-regulated genes should point to the biochemical features of the encoded proteins. 

Much as liquid water is essential for life, frozen water, ice, is frequently lethal, especially if ice formation occurs within the cell. Upon formation of ice, loss of liquid water may impair or preclude the four basic water-related functions listed above. In particular, the structures and the activities of macromolecules and membranes may be severely damaged. In fact, the harmful effects of ice formation are due to a suite of physical and chemical effects. Physical damage from ice crystals that form within a cell can lead to rupture of membranes and the consequent dissipation of concentration gradients between the cell and external fluids or between membrane-bounded compartments within the cell. Ice formation in the extracellular fluids also can lead to damage to membranes as well as to lethal dehydration of the cell, as water moves down its concentration gradient from the intracellular space to the now depleted pool of liquid water in the extracellular space. Dehydration of the cell not only deprives it of water, but also leads to harmful and perhaps lethal increases in the concentrations of inorganic ions, which remain behind in the cell. Because the activities and structures of nucleic acids and proteins are affected by the concentrations of ions in their milieu, dehydration is expected to lead to perturbation of macromolecular structure and metabolic activity. It should come as no surprise, therefore, that with rare exceptions such as the fat body cells of certain cold-tolerant insects (Lee et al., 1993b Salt, 1962), ice formation within cells is lethal. 

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