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J Exp Bot. 2014 Mar;65(5):1361-75. doi: 10.1093/jxb/ert460. Epub 2014 Jan 13.

Deciphering early events involved in hyperosmotic stress-induced programmed cell death in tobacco BY-2 cells.

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Université Paris Diderot, Sorbonne Paris Cité, Institut des Energies de Demain (UMR8236), Paris, France.


Hyperosmotic stresses represent one of the major constraints that adversely affect plants growth, development, and productivity. In this study, the focus was on early responses to hyperosmotic stress- (NaCl and sorbitol) induced reactive oxygen species (ROS) generation, cytosolic Ca(2+) concentration ([Ca(2+)]cyt) increase, ion fluxes, and mitochondrial potential variations, and on their links in pathways leading to programmed cell death (PCD). By using BY-2 tobacco cells, it was shown that both NaCl- and sorbitol-induced PCD seemed to be dependent on superoxide anion (O2·(-)) generation by NADPH-oxidase. In the case of NaCl, an early influx of sodium through non-selective cation channels participates in the development of PCD through mitochondrial dysfunction and NADPH-oxidase-dependent O2·(-) generation. This supports the hypothesis of different pathways in NaCl- and sorbitol-induced cell death. Surprisingly, other shared early responses, such as [Ca(2+)]cyt increase and singlet oxygen production, do not seem to be involved in PCD.


Calcium; NaCl; Nicotiana tabacum; hyperosmotic stress; mitochondria; non-selective cation channels; programmed cell death; reactive oxygen species.

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