Heat-Shock-Induced Changes in Intracellular Ca(2+) Level in Tobacco Seedlings in Relation to Thermotolerance

Exposure of plants to elevated temperatures results in a complex set of changes in gene expression that induce thermotolerance and improve cellular survival to subsequent stress. Pretreatment of young tobacco (Nicotiana plumbaginifolia) seedlings with Ca(2+) or ethylene glycol-bis(β-aminoethylether)-N,N,N′,N′-tetraacetic acid enhanced or diminished subsequent thermotolerance, respectively, compared with untreated seedlings, suggesting a possible involvement of cytosolic Ca(2+) in heat-shock (HS) signal transduction. Using tobacco seedlings transformed with the Ca(2+)-sensitive, luminescent protein aequorin, we observed that HS temperatures induced prolonged but transient increases in cytoplasmic but not chloroplastic Ca(2+). A single HS initiated a refractory period in which additional HS signals failed to increase cytosolic Ca(2+). However, throughout this refractory period, seedlings responded to mechanical stimulation or cold shock with cytosolic Ca(2+) increases similar to untreated controls. These observations suggest that there may be specific pools of cytosolic Ca(2+) mobilized by heat treatments or that the refractory period results from a temporary block in HS perception or transduction. Use of inhibitors suggests that HS mobilizes cytosolic Ca(2+) from both intracellular and extracellular sources.