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Programmed cell death (PCD) is a fundamental cellular process observed in eukaryotic cells of different origin (Huh et al., 2002; Buss et al., 2006; Piszczek and Gutman, 2007; Lam, 2008). Being an ordered series of events, PCD facilitates the removal of redundant, misplaced, or damaged cells and is essential for cellular differentiation and tissue homeostasis (Hoeberichts and Woltering, 2003; Chen and Dickman, 2004). Phloem differentiation, root cap and aerenchyma formation, aleurone and endosperm cell death, and leaf senescence are all known examples of PCD in plants. PCD is often associated with the occurrence of specific biochemical and morphological features such as condensation of the nucleus and cytoplasm, fragmentation of genomic DNA (‘DNA laddering’) and fragmentation of the cell into membrane-contained vesicles (apoptotic bodies) (Hoeberichts and Woltering, 2003). Other typical hallmarks of PCD in plants are an increase in caspase-like proteolytic activity and cytochrome c release from mitochondria. Being essential for cell and tissue homeostasis and specialization, PCD also plays an important role in mediating plant adaptive responses to the environment. The most characterized type of PCD in plants is a hypersensitive response (HR) observed in plants in response to pathogen attack (Pennell and Lamb, 1997; Lam et al., 2001). Recently, PCD has also been proved to occur in response to various abiotic stresses such as salinity, cold stress, waterlogging, and hypoxia (Katsuhara and Kawasaki, 1996; Drew et al., 2000; Kratsch and Wise, 2000; Huh et al., 2002). In contrast to the relatively well-described cell death pathway in animals, often referred to as apoptosis, mechanisms and regulation of plant PCD are still ill-defined (Hoeberichts and Woltering, 2003). It appears that the mechanism of DNA laddering varies in different species or even in different tissues of one organism (Jiang et al., 2008). A key role for caspase-like proteases has been suggested (Piszczek and Gutman, 2007), although caspase-encoding genes are not found in plants at the nucleotide sequence level (Hatsugai et al., 2004; Chichkova et al., 2004). In this issue, Affenzeller and colleagues report salinityinduced PCD in a freshwater green algae Micrasterias denticulata. They have shown that prolonged salt stress (24 h) led to degradation of organelles by autophagy, a special form of PCD where organelles are degenerated and enclosed by membranous structures derived from ER. This finding extends the phenomenon of salinity-induced PCD, previously reported in higher plants (Katsuhara and Kawasaki, 1996; Katsuhara, 1997; Katsuhara and Shibasaka, 2000; Lin et al., 2005; Li et al., 2007a, b) and yeasts (Huh et al., 2002), to algal species. Importantly, DNA laddering, one of the hallmarks of PCD, was visible as soon as 1 h after the onset of NaCl stress (Affenzeller et al., 2009) while previous reports suggested that at least 4 h of salinity treatment was needed (Li et al., 2007a). Another important aspect of Affenzeller and his colleagues’ work was the finding that the observed DNA laddering occurred in NaCl but not in sorbitol-stressed cells. This indicates that the ionic rather then the osmotic component of salt stress led to the activation of the endonuclease resulting in PCD. To the best of my knowledge, the only previous report on such ionic specificity of PCD was by Huh et al. (2002). Although the exact mechanisms beyond this specificity remain elusive, several lines of evidence suggest that changes in the cytosolic K/ Na ratio may be crucial for triggering PCD in living cells. Under saline conditions, strong membrane depolarization caused by Na uptake favours K efflux via depolarization-activated outward-rectifying K channels (Shabala et al., 2006). By contrast, isotonic mannitol or sorbitol solution causes significant membrane hyperpolarization, resulting in increased K uptake (Shabala et al., 2000; Shabala and Lew, 2002). This will result in a dramatic difference in cytosolic K level between these two types of stresses (Shabala and Cuin, 2008). In animal tissues, caspase activity is significantly increased by a low cytosolic K content (Hughes and Cidlowski, 1999). Assuming plant caspase-like proteases are regulated in a similar way, a decrease in the cytosolic K pool will activate caspase-like proteases leading to PCD after NaCl but not sorbitol treatment. Second, no DNA laddering was detected by Affenzeller and co-authors in 0.5 mM Zn-pretreated cells exposed to

Salinity and programmed cell death: unravelling mechanisms for ion specific signalling