INHIBITION OF PROGRAMMED CELL-DEATH IN TOBACCO PLANTS DURING A PATHOGEN-INDUCED HYPERSENSITIVE RESPONSE AT LOW-OXYGEN PRESSURE

The hypersensitive response (HR) of plants to invading pathogens is th ought to involve a coordinated activation of plant defense mechanisms and programmed cell death (pcd). To date, little is known about the me chanism underlying death of plant cells during this response. In addit ion, it is not known whether suppression of pcd affects the induction of other defense mechanisms during the HR. Here, we report that death of tobacco cells (genotype NN) infected with tobacco mosaic virus (TMV ) is inhibited at low oxygen pressure. In contrast, virus replication and activation of defense mechanisms, as measured by synthesis of the pathogenesis-related protein PR-1a, were not inhibited at low oxygen p ressure. Bacterium-induced pcd was also inhibited at low oxygen pressu re. However, pcd induced by TMV or bacteria was not inhibited in trans genic tobacco plants expressing the mammalian anti-pcd protein Bcl-X(L ). Our results suggest that ambient oxygen levels are required for eff icient pcd induction during the HR of plants and that activation of de fense responses can be uncoupled from cell death. Furthermore, pcd tha t occurs during the interaction of tobacco with TMV or bacteria may be distinct from some cases of pcd or apoptosis in animals that are inse nsitive to low oxygen or inhibited by the Bcl-X(L) protein.