Abstract
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 Ca2+ concentration ([Ca2+]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 [Ca2+]cyt increase and singlet oxygen production, do not seem to be involved in PCD.
Highlights
Salt stress is known to have severe effects on plant growth and development (Tester and Davenport, 2003)
These shifts in osmolality induced by 400 mM sorbitol or 200 mM NaCl led to the death of a part of the cell population, dead cells displaying large cell shrinkage (Fig. 1A), the hallmark of the programmed cell death (PCD) process
In order to confirm whether this cell death was due to an active process requiring active gene expression and cellular metabolism, Bright Yellow 2 (BY-2) cell suspensions were treated with actinomycin D (AD), an inhibitor of RNA synthesis, or with cycloheximide (Chx), an inhibitor of protein synthesis, each at 20 mg ml–1, 15 min prior to 200 mM NaCl or 400 mM sorbitol exposure
Summary
Salt stress is known to have severe effects on plant growth and development (Tester and Davenport, 2003). High salinity leads to ionic, osmotic, and oxidative stress in plants (Zhu, 2001) that may result in the induction of signalling events that lead to programmed cell death (PCD) in higher plants (Huh et al, 2002; Lin et al, 2006; Shabala, 2009; Wang et al, 2010) and algae (Affenzeller et al, 2009). Such PCD could be regarded as a salt adaptation mechanism (Huh et al, 2002).
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