VIEW ARTICLE | DOI: 10.1094/MPMI-5-372
Disease Development in Ethylene-Insensitive Arabidopsis thaliana Infected with Virulent and Avirulent Pseudomonas and Xanthomonas Pathogens. Andrew F. Bent. Department of Plant Pathology, University of California, Berkeley 94720 U.S.A. Roger W. Innes(1), Joseph R. Ecker(2), and Brian J. Staskawicz(1). (1)Department of Plant Pathology, University of California, Berkeley 94720 U.S.A. and (2)Plant Science Institute, Department of Biology, University of Pennsylvania, Philadelphia 19104-6018 U.S.A. MPMI 5:372-378. Accepted 29 June 1992. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1992.
Additional Keywords: etol, etrl.
The plant hormone ethylene has been hypothesized to play roles both in disease resistance and in disease susceptibility. These processes were examined by using isogenic virulent and avirulent bacterial pathogens and mutants of Arabidopsis thaliana that were altered in ethylene physiology. Ethylene-insensitive ein1 and ein2 mutants of Arabidopsis were resistant to Pseudomonas syringae pv. tomato made avirulent by the addition of the cloned avirulence genes avrRpt2, avrRpm1, or avrB; this suggests that ethylene is not required for active resistance against avirulent bacteria. In a second set of experiments, susceptibility was monitored with virulent P. s. pv. tomato, P. s. pv. maculicola, or Xanthomonas campestris pv. campestris strains. Wild-type Arabidopsis and ein1 mutants were susceptible to these strains, but ein2 mutants developed only minimal disease symptoms. Despite these reduced symptoms, virulent P. s. pv. tomato grew extensively within ein2 leaves. The Pseudomonas phytotoxin coronatine induces ethylene biosynthesis and diseaselike symptoms on many plant species, but the reduced symptomology of ein2 mutants could not be attributed to insensitivity to coronatine. The enhanced disease tolerance of ein2 plants suggests that ethylene may mediate pathogen-induced damage, but the absence of tolerance in ein1 mutants has yet to be explained.