R. Tenhaken et C. Rubel, SALICYLIC-ACID IS NEEDED IN HYPERSENSITIVE CELL-DEATH IN SOYBEAN BUT DOES NOT ACT AS A CATALASE INHIBITOR, Plant physiology, 115(1), 1997, pp. 291-298
The function of salicylic acid (SA) in hypersensitive cell death was s
tudied in a soybean (Glycine max)-Pseudomonas syringae pv glycinea sys
tem. The infection of cell cultures with bacteria leads to a hypersens
itive reaction (HR), which is dependent on an appropriate avirulence g
ene and on low concentrations of SA. The requirement for SA is essenti
al for a process shortly before the onset of the HR-caused cell death
5 to 6 h after infection with bacteria. SA given 10 to 12 h after infe
ction or preincubation cannot rescue the completion of the cell death
program. SA does not inhibit catalase or ascorbate peroxidase in soybe
an. In addition, the in vivo capacity of the cell culture for the rapi
d metabolism of H2O2 is not altered by SA. This clearly shows that SA
is needed for the HR-caused cell death for a reaction downstream of th
e oxidative burst. Lipid peroxides accumulate during the HR, but the l
oss of membrane control precedes the generation of lipid peroxides. Th
e accumulation of lipid peroxides in the HR can be prevented by lipid
antioxidants. Nevertheless, cell death kinetics remain unaltered in th
e presence of antioxidants. It is concluded that lipid peroxides are a
consequence of cell death, but not the primary cause of it.