The Arabidopsis PAD4 gene was previously shown to be required for synt
hesis of camalexin in response to infection by the virulent bacterial
pathogen Pseudomonas syringae pv maculicola ES4326 but not in response
to challenge by the non-host fungal pathogen Cochliobolus carbonum, I
n this study, we show that pad4 mutants exhibit defects in defense res
ponses, including camalexin synthesis and pathogenesis-related PR-1 ge
ne expression, when infected by P. s. maculicola ES4326. No such defec
ts were observed in response to infection by an isogenic avirulent str
ain carrying the avirulence gene avrRpt2. In P s. maculicola ES4326-in
fected pad4 plants, synthesis of salicylic acid (SA) was found to be r
educed and delayed when compared with SA synthesis in wild-type plants
. Moreover, treatment of pad4 plants with SA partially reversed the ca
malexin deficiency and PR-1 gene expression phenotypes of P. s. maculi
cola ES4326-infected pad4 plants. These findings support the hypothesi
s that PAD4 acts upstream from SA accumulation in regulating defense r
esponse expression in plants infected with P. s. maculicola ES4326. A
working model of the role of PAD4 in governing expression of defense r
esponses is presented.