An heuristic hypothesis of chilling injury in plants: a role for calcium as the primary physiological transducer of injury

Abstract

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.