In Arabidopsis, the rhizobacterial strain Pseudomonas fluorescens WCS417r triggers jasmonate (JA)- and
ethylene (ET)-dependent induced systemic resistance (ISR) that is effective against different pathogens.
Arabidopsis genotypes unable to express rhizobacteria-mediated ISR against the bacterial pathogen
Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) exhibit enhanced disease susceptibility towards
this pathogen. To identify novel components controlling induced resistance, we tested 11 Arabidopsis
mutants with enhanced disease susceptibility (eds) to pathogenic P. syringae bacteria for WCS417rmediated
ISR and pathogen-induced systemic acquired resistance (SAR). Mutants eds4-1, eds8-1 and
eds10-1 failed to develop WCS417r-mediated ISR, while mutants eds5-1 and eds12-1 failed to express
pathogen-induced SAR. Whereas eds5-1 is known to be blocked in salicylic acid (SA) biosynthesis,
analysis of eds12-1 revealed that its impaired SAR response is caused by reduced sensitivity to this
molecule. Analysis of the ISR-impaired eds mutants revealed that they are non-responsive to induction
of resistance by methyl jasmonate (MeJA) (eds4-1, eds8-1 and eds10-1), or the ET precursor 1-
aminocyclopropane-1-carboxylate (ACC) (eds4-1 and eds10-1). Moreover, eds4-1 and eds8-1 showed
reduced expression of the plant defensin gene PDF1.2 after MeJA and ACC treatment, which was
associated with reduced sensitivity to either ET (eds4-1) or MeJA (eds8-1). Although blocked in
WCS417r-, MeJA- and ACC-induced ISR, eds10-1 behaved normally for several other responses to MeJA
or ACC. The results indicate that EDS12 is required for SAR and acts downstream of SA, whereas EDS4,
EDS8 and EDS10 are required for ISR acting either in JA signalling (EDS8), ET signalling (EDS4), or
downstream JA and ET signalling (EDS10) in the ISR pathway
