Myo-inositol abolishes salicylic acid-dependent cell death and pathogen defence responses triggered by peroxisomal hydrogen peroxide.

• Signalling between reactive oxygen species (ROS) and salicylic acid (SA)-dependent programmed cell death (PCD) and defence responses is complex and much remains to be discovered. Recent reports have implicated myo-inositol (MI) in defence responses, but the relationships between MI, ROS and SA remain to be elucidated. • This question was investigated in catalase-deficient Arabidopsis thaliana plants (cat2), in which a peroxisomal H(2) O(2) trigger induces SA-dependent lesion formation and a wide range of pathogen responses. • GC-MS analysis revealed that leaf MI contents were markedly decreased in cat2 independently of SA accumulation. Supplying MI to cat2 blocked lesion formation, SA accumulation and associated defence responses in a manner that closely mimicked the effect of genetically blocking SA synthesis through isochorismate synthase 1 (ICS1). The effects of MI were linked to repression of ICS1 transcripts but not decreased oxidative stress or signalling, and caused loss of resistance to virulent bacteria. The antagonistic effects of MI on lesion formation and resistance could be partly restored by supplying SA. • Our findings demonstrate a role for MI in cell death triggered by peroxisomal H(2) O(2) , and suggest that the tissue content of this compound is a key factor determining whether oxidative stress induces or opposes defence responses.