Salt stress-induced programmed cell death via Ca2+-mediated mitochondrial permeability transition in tobacco protoplasts

Abstract

The change in cytosolic free concentration of calcium ([Ca2+]cyt) plays a key role in regulating apoptosis in animal cells. In our experiment, we tried to investigate the function of Ca2+ in programmed cell death (PCD) in tobacco (Nicotiana tobacum, cultivar BY-2) protoplasts induced by salt stress. An obvious increase in [Ca2+]cyt was observed a few minutes after treatment and the onset of a decrease in mitochondrial membrane potential (ΔΨm) was also observed before the appearance of PCD, pre-treatment of protoplasts with EGTA or LaCl3 effectively retarded the increase in [Ca2+]cyt, which was concomitant with the decrease in the percentage of cell death and higher ΔΨm, pre-treatment with cyclosporine A (CsA) also effectively retarded the increase in [Ca2+]cyt, the decrease in ΔΨm and the onset of PCD. All these results suggest that Ca2+ is a necessary element in regulating PCD and the increase in [Ca2+]cyt and the opening of mitochondrial permeability transition pore (MPTP) could promote each other in regulating PCD in tobacco protoplasts induced by salt stress.