Systemic acquired resistance (SAR) is an inducible plant defense respo
nse in which a prior foliar pathogen infection activates resistance in
noninfected foliar tissues. Salicylic acid (SA) accumulation is essen
tial for the establishment of SAR. While SA is probably not the long-d
istance systemic signal instrumental for SAR activation, it is require
d for transduction of the signal in noninfected tissues. Although SAR
was first described as a response to necrogenic pathogen infection, sy
nthetic chemicals have been identified that effectively activate SAR.
Elucidation of SAR signal transduction has been facilitated by the ide
ntification and characterization of Arabidopsis mutants. Disease lesio
n mimic mutants exhibit constitutive SAR as well as spontaneous lesion
formation similar to pathogen-associated hypersensitive cell death. S
ome disease lesion mimic mutants do not exhibit a lesioned phenotype w
hen SA accumulation is prevented, thereby providing evidence for a fee
dback loop in SAR signal transduction. Moreover, characterization of m
utants compromised for SAR activation has provided additional evidence
for common signaling components between SAR and gene-for-gene resista
nce.