Expression of animal CED-9 anti-apoptotic gene in tobacco modifies plasma membrane ion fluxes in response to salinity and oxidative stress.

Apoptosis, one form of programmed cell death (PCD), plays an important role in mediating plant adaptive responses to the environment. Recent studies suggest that expression of animal anti-apoptotic genes in transgenic plants may significantly improve a plant's ability to tolerate a variety of biotic and abiotic stresses. The underlying cellular mechanisms of this process remain unexplored. In this study, we investigated specific ion flux "signatures" in Nicotiana benthamiana plants transiently expressing CED-9 anti-apoptotic gene and undergoing salt- and oxidative stresses. Using a range of electrophysiological techniques, we show that expression of CED-9 increased plant salt and oxidative stress tolerance by altering K(+) and H(+) flux patterns across the plasma membrane. Our data shows that PVX/CED-9 plants are capable of preventing stress-induced K(+) efflux from mesophyll cells, so maintaining intracellular K(+) homeostasis. We attribute these effects to the ability of CED-9 to control at least two types of K(+)-permeable channels; outward-rectifying depolarization-activating K(+) channels (KOR) and non-selective cation channels (NSCC). A possible scenario linking CED-9 expression and ionic relations in plant cell is suggested. To the best of our knowledge, this study is the first to link "ion flux signatures" and mechanisms involved in regulation of PCD in plants.