In our previous studies (Chae et al., 1990; Chae et ol., 1993), we found that a phytochrome signal was clearly connected with the change in cytosolic free Ca^(2+) concentrntion ([Ca^(2+)]_i) in oat cells. It was determined that the [Ca^(2+)]_i change ...
In our previous studies (Chae et al., 1990; Chae et ol., 1993), we found that a phytochrome signal was clearly connected with the change in cytosolic free Ca^(2+) concentrntion ([Ca^(2+)]_i) in oat cells. It was determined that the [Ca^(2+)]_i change occured both by mobilization out of the intracellular Ca^(2+) store and by influx from the medium. The specific aim of this work is to elucidate the processes connecting Ca^(2+) mobilization and influx. The cells treated with thapsigargin (increasing [Ca^(2+)]_i by inhibition of the Ca^(2+)-ATPase in the calcium pool) in the presence of external Ca^(2+) showed the same increasing pattern (sustained increasing shape) of [Ca^(2+)]_i as that measured in animal cells. Red light irradiation after thapsigargin treatment did not increase [Ca^(2+)]_i. These results suggest that thapsigargin also acts specifically in the processes of mobilization and influx of Ca^(2+) in oat cells. When the cells were treated with TEA (K^+ channel blocker), changes in [Ca^(2+)]_i were drastically reduced in comparison with that measured in the absence of TEA. The results suggest that the change in [Ca^(2+)]_i due to red light irradiation is somehow related with K^+ channel opening to change membrane potential. The membrane potential change due to K^+ influx might be the critical factor in opening a voltage-dependent calcium channel for Ca^(2+) influx.