Separate jasmonate-dependent and salicylate-dependent defense-response pathways in Arabidopsis are essential for resistance to distinct microbial pathogens
Bphj. Thomma et al., Separate jasmonate-dependent and salicylate-dependent defense-response pathways in Arabidopsis are essential for resistance to distinct microbial pathogens, P NAS US, 95(25), 1998, pp. 15107-15111
Citations number
32
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
The endogenous plant hormones salicylic acid (SA) and jasmonic acid (JA), w
hose levels increase on pathogen infection, activate separate sets of genes
encoding antimicrobial proteins in Arabidopsis thaliana. The pathogen-indu
cible genes PR-1, PR-2, and PR-5 require SA signaling for activation, where
as the plant defensin gene PDF1.2, along with a PR-3 and PR-4 gene, are ind
uced by pathogens via an SA-independent and JA-dependent pathway. An Arabid
opsis mutant, coil, that is affected in the JA-response pathway shows enhan
ced susceptibility to infection by the fungal pathogens Alternaria brassici
cola and Botrytis cinerea but not to Peronospora parasitica, and vice versa
for two Arabidopsis genotypes (npr1 and NahG) with a defect in their SA re
sponse. Resistance to P. parasitica was boosted by external application of
the SA-mimicking compound 2,6-dichloroisonicotinic acid [Delaney, T., et al
. (1994) Science 266, 1247-1250] but not by methyl jasmonate (MeJA), wherea
s treatment with MeJA but not 2,6-dichloroisonicotinic acid elevated resist
ance to Alternaria brassicicola. The protective effect of MeJA against A. b
rassicicola was the result of an endogenous defense response activated ira
planta and not a direct effect of MeJA on the pathogen, as no protection to
A. brassicicola was observed in the coil mutant treated with MeJA. These d
ata point to the existence of at least two separate hormone-dependent defen
se pathways in Arabidopsis that contribute to resistance against distinct m
icrobial pathogens.