Activation of the plant defensin gene PDF1.2 in Arabidopsis by pathogens has been shown previously to be blocked in the ethylene response mutant ein2-1 and the jasmonate response mutant coi1-1. In this work, we have further investigated the interactions between the ethylene and jasmonate signal pathways for the induction of this defense response. Inoculation of wild-type Arabidopsis plants with the fungus Alternaria brassicicola led to a marked increase in production of jasmonic acid, and this response was not blocked in the ein2-1 mutant. Likewise, A. brassicicola infection caused stimulated emission of ethylene both in wild-type plants and in coi1-1 mutants. However, treatment of either ein2-1 or coi1-1 mutants with methyl jasmonate or ethylene did not induce PDF1.2 , as it did in wild-type plants. We conclude from these experiments that both the ethylene and jasmonate signaling pathways need to be triggered concomitantly, and not sequentially, to activate PDF1.2 upon pathogen infection. In support of this idea, we observed a marked synergy between ethylene and methyl jasmonate for the induction of PDF1.2 in plants grown under sterile conditions. In contrast to the clear interdependence of the ethylene and jasmonate pathways for pathogen-induced activation of PDF1.2 , functional ethylene and jasmonate signaling pathways are not required for growth responses induced by jasmonate and ethylene, respectively.
INTRODUCTIONHigher plants induce various defense responses when they are attacked by microbial pathogens, such as fungi, bacteria, or viruses. These defense responses include suicide of the attacked host cell (the so-called hypersensitive response); the production of antimicrobial secondary metabolites (called phytoalexins); the production of pathogenesisrelated (PR) proteins, of which many exert antimicrobial properties; and the production and oxidative cross-linking of cell wall polymers. The efficacy of these defense responses often determines whether plants are susceptible to infection by a pathogen.Elicitors secreted by or released from microbial invaders are the primary signal for induction of plant defense responses (Ebel and Cosio, 1994). Each pathogen produces a particular mixture of elicitors, which are sometimes accompanied by suppressors, and these molecules interact with receptors on the host cells that further translate the primary signal into particular events in the plasma membrane, the cytosol, and/or the nucleus (Shirasu et al., 1996). Induction of some defense genes requires the generation of secondary endogenous signal molecules (stress hormones) by the challenged cells in the infection site. The secondary signal molecules in turn set in motion signal transduction cascades in receiving cells, eventually leading to activation of pathogen-responsive genes. Secondary signal molecules thus serve to amplify and spread the response of the host after initial recognition of the pathogen. Several secondary signal molecules whose synthesis is increased in response to elicitor recognition and that ar...