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THE PLANT CELL, Vol 8, Issue 2 203-212, Copyright © 1996 by American Society of Plant Biologists
Production of Salicylic Acid Precursors Is a Major Function of Phenylalanine Ammonia-Lyase in the Resistance of Arabidopsis to Peronospora parasitica
B. Mauch-Mani and A. J. Slusarenko
Institute of Plant Biology, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland
Arabidopsis ecotype Columbia (Col-0) seedlings, transformed with a
phenylalanine ammonia-lyase 1 promoter (PAL1)-[beta]-glucuronidase (GUS)
reporter construct, were inoculated with virulent and avirulent isolates of
Peronospora parasitica. The PAL1 promoter was constitutively active in the
light in vascular tissue but was induced only in the vicinity of fungal
structures in the incompatible interaction. A double-staining procedure was
developed to distinguish between GUS activity and fungal structures. The
PAL1 promoter was activated in cells undergoing lignification in the
incompatible interaction in response to the pathogen. Pretreatment of the
seedlings with 2-aminoindan-2-phosphonic acid (AIP), a highly specific PAL
inhibitor, made the plants completely susceptible. Lignification was
suppressed after AIP treatment, and surprisingly, pathogen-induced PAL1
promoter activity could not be detected. Treatment of the seedlings with
2-hydroxyphenylaminosulphinyl acetic acid (1,1-dimethyl ester) (OH-PAS), a
cinnamyl alcohol dehydrogenase inhibitor specific for the lignification
pathway, also caused a shift toward susceptibility, but the effect was not
as pronounced as it was with AIP. Significantly, although OH-PAS suppressed
pathogen-induced lignification, it did not suppress pathogen-induced PAL1
promoter activation. Salicylic acid (SA), supplied to AIP-treated plants,
restored resistance and both pathogen-induced lignification and activation
of the PAL1 promoter. Endogenous SA levels increased significantly in the
incompatible but not in the compatible combination, and this increase was
suppressed by AIP but not by OH-PAS. These results provide evidence of the
central role of SA in genetically determined plant disease resistance and
show that lignification per se, although providing a component of the
resistance mechanism, is not the deciding factor between resistance and
susceptibility.
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