Low temperature is an important environmental factor that greatly influences the growth, development, survival, and geographical distribution of plants (Levitt 1980). Whereas most plant species from temperate regions can acclimatize to cold and can survive exposures to deep freezing temperatures, plants of tropical and subtropical origin are severely injured when exposed to low nonfreezing temperatures between 0 and 15°C (Lyons 1973; Lynch 1990; Wang 1990). Symptoms of chilling injury often include cessation of growth, wilting, chlorosis, necrosis, and eventually plant death (Lyons 1973; Graham and Patterson 1982; Maruyama et al. 1990; Allen and Ort 2001) . In addition to its adverse effects on plant growth and development, chilling sensitivity also imposes major limitations on the posthar-vest storage and handling of many fruits and vegetables, because it necessitates storage at relatively high temperatures that do little to delay deterioration and spoilage (Paull 1990) .

In contrast to our knowledge of plant responses to other abiotic stresses, such as freezing, drought, salinity, and heat, little is known regarding the molecular basis in regulating chilling tolerance or about the signal transduction networks involved in its acquisition. In previous reviews, the occurrence of chilling damage was attributed mainly to the general disruption or dysfunction of cellular metabolic processes (Lyons 1973 ; Graham and Patterson 1982; Markhart 1986). In this respect, it has been suggested that an important primary event in the occurrence of chilling injury is an alteration in the physical state of the cellular membranes, which leads to dysfunctional selective permeability and increases in solute leakage from the cells (Lyons 1973; Markhart 1986; Nishida and Murata 1996). Another factor that affects susceptibility to chilling is the status of the cellular antioxidant defensive system required to avoid accumulation of toxic reactive oxygen species (ROS). Indeed, overexpression of anti-oxidant defensive genes, such as ascorbate per-oxidase, superoxide dismutase, and catalase (CAT) enhanced chilling tolerance (Van Breusegem et al. 1999; Payton et al. 2001), whereas repression of catalase gene expression reduced chilling tolerance (Kerdnaimongkol and Woodson 1999). Finally, several reports have suggested that various stress genes, usually related to other types of stress responses, may also contribute to the acquisition of chilling tolerance. For instance, it has been suggested that heat shock proteins (HSPs) (Sabehat et al. 1998) and dehydrin genes (Ismail et al. 1999) may also be factors in chilling tolerance in plants.

In this chapter, we will summarize data obtained from studies on Arabidopsis chilling-sensitive (chs) mutants, and will suggest how the adoption of Arabidopsis as a plant model system could improve our basic understanding regarding the molecular and biochemical nature of chilling tolerance. Overall, Arabidopsis has many advantages as a plant model system and its chilling tolerance makes it an excellent study subject for the identification of major genetic traits important for low temperature survival of plants.

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