We characterized the accumulation patterns of Arabidopsis thaliana proteins
, two CuZnSODs, FeSOD, MnSOD, PR1, PR5, and GST1, in response to various pa
thogen-associated treatments, These treatments included inoculation with vi
rulent and avirulent Pseudomonas syringae strains, spontaneous lesion forma
tion in the lsd1 mutant, and treatment with the salicylic acid (SA) analogs
INA (2,6-dichloroisonicotinic acid) and BTH (benzothiadiazole), The PR1, P
R5, and GST1 proteins were inducible by all treatments tested, as expected
from previous mRNA blot analysis. The two CuZnSOD proteins were induced by
SA analogs and in conjunction with lsd1-mediated spreading cell death, Addi
tionally, LSD1 is a part of a signaling pathway for the induction of the Cu
ZnSOD proteins in response to SA but not in lsd1-mediated cell death. We su
ggest that the spreading lesion phenotype of lsd1 results from a lack of up
-regulation of a CuZnSOD responsible for detoxification of accumulating sup
eroxide before the reactive oxygen species can trigger a cell death cascade
.