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THE PLANT CELL, Vol 3, Issue 8 809-818, Copyright © 1991 by American Society of Plant Biologists
Salicylic Acid Is a Systemic Signal and an Inducer of Pathogenesis-Related Proteins in Virus-Infected Tobacco
N. Yalpani, P. Silverman, TMA. Wilson, D. A. Kleier and I. Raskin
AgBiotech Center, Cook College, Rutgers University, P.O. Box 231, New Brunswick, New Jersey 08903-0231
Systemic induction of pathogenesis-related (PR) proteins in tobacco, which
occurs during the hypersensitive response to tobacco mosaic virus (TMV),
may be caused by a minimum 10-fold systemic increase in endogenous levels
of salicylic acid (SA). This rise in SA parallels PR-1 protein induction
and occurs in TMV-resistant Xanthi-nc tobacco carrying the N gene, but not
in TMV-susceptible (nn) tobacco. By feeding SA to excised leaves of
Xanthi-nc (NN) tobacco, we have shown that the observed increase in
endogenous SA levels is sufficient for the systemic induction of PR-1
proteins. TMV infection became systemic and Xanthi-nc plants failed to
accumulate PR-1 proteins at 32[deg]C. This loss of hypersensitive response
at high temperature was associated with an inability to accumulate SA.
However, spraying leaves with SA induced PR-1 proteins at both 24 and
32[deg]C. SA is most likely exported from the primary site of infection to
the uninfected tissues. A computer model predicts that SA should move
rapidly in phloem. When leaves of Xanthi-nc tobacco were excised 24 hr
after TMV inoculation and exudates from the cut petioles were collected,
the increase in endogenous SA in TMV-inoculated leaves paralleled SA levels
in exudates. Exudation and leaf accumulation of SA were proportional to TMV
concentration and were higher in light than in darkness. Different
components of TMV were compared for their ability to induce SA accumulation
and exudation: three different aggregation states of coat protein failed to
induce SA, but unencapsidated viral RNA elicited SA accumulation in leaves
and phloem. These results further support the hypothesis that SA acts as an
endogenous signal that triggers local and systemic induction of PR-1
proteins and, possibly, some components of systemic acquired resistance in
NN tobacco.
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