Short-term salinity stress in tobacco plants leads to the onset of animal-like PCD hallmarks in planta in contrast to long-term stress.

Recent results have identified mitochondria as centers of stress-induced generation of reactive oxygen species in plants. Depolarization of plant mitochondrial membrane during stress results the release of programmed cell death (PCD)-inducing factors in the cytosol in a fashion similar to the onset of animal-like PCD. Herein, we report significant similarities of animal-like PCD and salinity stress-induced plant PCD. Short-term salinity stress (3 h) led to depolarization of the mitochondrial membrane, release of cytochrome c (CYT-c), which was visualized using a contemporary molecular technique, activation of caspase-3 type proteases and the onset of PCD in wild type tobacco plants, Nicotiana tabacum cv. Petit Havana. However, PCD was not manifested during long-term salinity stress (24 h). Interestingly long-term salinity stress led to necrotic-like features, which were accompanied by collapse of respiration, reduction of key components of the respiratory chain, such as CYT-c and alternative oxidase, ATP depletion and high proteolytic activity. The results suggest that salinity stress of tobacco plants in planta leads to the onset of animal-like PCD only during the early stages post-stress, while long-term stress leads to necrotic-like features.