Abstract. It is suggested that increased levels of free cytosolic calcium ([Ca2+]cyt) may serve as the primary physiological transducer of chilling injury in plants. Numerous similarities between the effects of [Ca2+]cyt‐raising treatments on plants and the effects of chilling temperatures on chilling‐sensitive (CS) plants are noted. It is proposed that chilling temperatures may lead to increases in [Ca2+]cyt in CS plant cells by reducing the rate at which they exclude Ca2+ from their cytosol and that rapid cooling (coldshock) may cause rapid increases in [Ca2+]cyt due to the activation of voltage‐dependent cation channels. Chill‐induced increases in [Ca2+]cyt in the cells of CS plants may reflect either an inherent inability of such plants to maintain homeostatic levels of Ca2+ at low temperatures or a stress‐induced reaction which has evolved to enable such cells to cope more effectively with the short‐term hardships imposed by cold. Previous proposals concerning the physiological transduction of chilling injury are also discussed. It is argued that there is little evidence to suggest that the immediate effects of low temperatures on CS cells include either decreases in ATP levels, general increases in the passive permeability of membranes, or increased rates of fermentation.

Abstract. The different effects which fast versus slow cooling have on such fundamental plant processes as ion transport, protoplasmic streaming, phloem translocation, growth, cell motility, water absorption and membrane potential are reviewed. When plant cells are rapidly cooled to non‐injurious temperatures, many of the physiological ramifications of rapid‐cooling stimulation are only transiently observed. It is proposed that these transient rapid‐cooling‐induced responses, sometimes elicited by temperature drops of only a few degrees centigrade, are manifestations of temperature sensing. The hypothesis is advanced that graded potentials, produced in response to rapidly falling temperature, are associated with graded increases in cytosolic free calcium. These transient increases in cytosolic free calcium give rise to many of the physiological effects elicited by rapid cooling. Other effects, however, such as those associated with alterations in membrane composition, gene expression and post‐translational modifications of proteins, may persist longer. The questions of the possible physiological advantage of temperature sensing, and its implications for the study of chilling injury, are discussed.

Abstract. Rapid‐cooling pulses to non‐stressful temperatures cause strong, transient depolarizations in cortical cells of cucumber roots. The amplitudes of these electrical responses are graded according to the rate and amplitude of the cooling pulse. Such graded potentials are typical of sensory processes and indicate that plants possess the ability to sense temperature change. La3+, a blocker of Ca2+ channels, and ethylene glycol bis‐(β‐aminoethyl ether) N,N,N′,N′‐acetic acid (EGTA), a Ca2+ chelator, inhibit the electrical responses elicited by rapid‐cooling pulses. High external [Ca2+] enhances them. These results indicate the involvement of a plasma membrane‐associated Ca2+ channel in the process of temperature sensing by plants. Calmodulin antagonists prolong the repolarization phase of the electrical responses, suggesting a role for calmodulin in the recovery from stimulation.