Genetics, Vol. 156, 341-350, September 2000, Copyright © 2000

Uncoupling Salicylic Acid-Dependent Cell Death and Defense-Related Responses From Disease Resistance in the Arabidopsis Mutant acd5

Jean T. Greenberga, F. Paul Silvermanb, and Hua Lianga
a Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois 60637
b Valent Biosciences Corporation, Long Grove, Illinois 60647

Corresponding author: Jean T. Greenberg, Department of Molecular Genetics and Cell Biology, University of Chicago, 1103 East 57th St. EBC410, Chicago, IL 60637., jgreenbe{at}midway.uchicago.edu (E-mail)

Communicating editor: V. L. CHANDLER

Salicylic acid (SA) is required for resistance to many diseases in higher plants. SA-dependent cell death and defense-related responses have been correlated with disease resistance. The accelerated cell death 5 mutant of Arabidopsis provides additional genetic evidence that SA regulates cell death and defense-related responses. However, in acd5, these events are uncoupled from disease resistance. acd5 plants are more susceptible to Pseudomonas syringae early in development and show spontaneous SA accumulation, cell death, and defense-related markers later in development. In acd5 plants, cell death and defense-related responses are SA dependent but they do not confer disease resistance. Double mutants with acd5 and nonexpressor of PR1, in which SA signaling is partially blocked, show greatly attenuated cell death, indicating a role for NPR1 in controlling cell death. The hormone ethylene potentiates the effects of SA and is important for disease symptom development in Arabidopsis. Double mutants of acd5 and ethylene insensitive 2, in which ethylene signaling is blocked, show decreased cell death, supporting a role for ethylene in cell death control. We propose that acd5 plants mimic P. syringae-infected wild-type plants and that both SA and ethylene are normally involved in regulating cell death during some susceptible pathogen infections.




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