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THE PLANT CELL, Vol 9, Issue 2 261-270, Copyright © 1997 by American Society of Plant Biologists
Salicylic Acid Potentiates an Agonist-Dependent Gain Control That Amplifies Pathogen Signals in the Activation of Defense Mechanisms
K. Shirasu, H. Nakajima, V. K. Rajasekhar, R. A. Dixon and C. Lamb
Plant Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037
The phenylpropanoid-derived natural product salicylic acid (SA) plays a key
role in disease resistance. However, SA administered in the absence of a
pathogen is a paradoxically weak inductive signal, often requiring
concentrations of 0.5 to 5 mM to induce acquired resistance or related
defense mechanisms or to precondition signal systems. In contrast,
endogenous SA accumulates to concentrations of <70 [mu] at the site of
attempted infection. Here, we show that although 10 to 100 [mu] SA had
negligible effects when administered to soybean cell suspensions in the
absence of a pathogen, physiological concentrations of SA markedly enhanced
the induction of defense gene transcripts, H2O2 accumulation, and
hypersensitive cell death by an avirulent strain of Pseudomonas syringae pv
glycinea, with optimal effects being at ~50 [mu]M. SA also synergistically
enhanced H202 accumulation in response to the protein phosphatase type 2A
inhibitor cantharidin in the absence of a pathogen. The synergistic effect
of SA was potent, rapid, and insensitive to the protein synthesis inhibitor
cycloheximide, and we conclude that SA stimulates an agonist-dependent gain
control operating at an early step in the signal pathway for induction of
the hypersensitive response. This fine control mechanism differs from
previously described time-dependent, inductive coarse control mechanisms
for SA action in the absence of a pathogen. Induction of H202 accumulation
and hypersensitive cell death by avirulent P. s. glycinea was blocked by
the phenylpropanoid synthesis inhibitor
[alpha]-aminooxy-[beta]-phenylpropionic acid, and these responses could be
rescued by exogenous SA. Because the agonist-dependent gain control
operates at physiological levels of SA, we propose that rapid fine control
signal amplification makes an important contribution to SA function in the
induction of disease resistance mechanisms.
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