First, third, fourth, and fifth authors: Laboratoire de Biologie Moléculaire des Relations Plantes-Microorganismes, CNRS/INRA, Chemin de Borde-Rouge, BP 27, Castanet-Tolosan, 31326, France; and second author: Max-Planck-Institut für Züchtungsforschung, Abteilung Biochemie, Carl von Linné Weg 10, D-50829 Köln, Germany
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Accepted for publication 6 June 2002.
Wilt disease caused by the phytopathogenic bacterium Ralstonia solanacearum is poorly understood at the molecular level. The possible roles of salicylic acid, jasmonic acid, and ethylene, compounds commonly associated with the plant response to pathogens, in wilt symptom development were investigated using various Arabidopsis thaliana mutants in a Col-0 background, an ecotype that develops wilt symptoms in response to the virulent GMI1000 strain. Following root inoculation, wilt symptoms were delayed in ein2-1, an ethylene-insensitive mutant, in response to several virulent strains of the pathogen. In ein2-1, bacteria invade the plant and multiply, reaching concentrations slightly lower than those detected in susceptible plants but 1 to 2 logs higher than in Nd-1, an A. thaliana ecotype resistant to strain GMI1000. This delay in disease symptom development of ein2-1 plants suggests that ethylene signaling plays a critical role in wilt disease development. Furthermore, a strong accumulation of transcripts corresponding to PR-3 and PR-4, two ethylene-responsive genes, was observed in susceptible Col-0 plants, but not in ein2-1 and Nd-1 plants, providing additional evidence for a role of ethylene in wilt symptom production. However, this hormone is probably not involved in the establishment of resistance to R. solanacearum, because homozygous ein2-1 plants in a resistant background remain fully resistant to strain GMI1000.
© 2002 The American Phytopathological Society