Soybean cell cultures (cv. Williams 82) respond to Pseudomonas syringae bac
teria expressing the avirulence gene AvrA with a hypersensitive reaction, a
programmed cell death (PCD) of plant cells to pathogen attack. This PCD is
under control of salicylic acid (SA) via an unknown mechanism. In the pres
ence of low concentrations of SA, the cells undergo a very rapid cell death
, which needs only half of the time required for the normal hypersensitive
reaction (HR). Northern blot studies for defence-related genes show that th
e expression of many of these genes is tightly linked to the status of the
cell death program rather than to pathogen-derived elicitors. Thus the expr
ession is much faster in the SA-accelerated PCD than in the normal hypersen
sitive reaction. In contrast, other pathogen-responsive genes are induced i
ndependently of the speed of PCD, indicating a divergent signalling mechani
sm. The production of reactive oxygen species during the oxidative burst of
bacteria-inoculated soybean cells is slightly enhanced in the presence of
SA but occurs at the same time as in untreated cells, suggesting that SA ex
hibits the control of the PCD downstream of the oxidative burst. Consistent
with these findings a HR-specific marker gene is neither directly induced
by H2O2 or SA. However, this gene shows a high expression in the regular HR
and is induced much faster in the SA-accelerated PCD.