Peroxisomal Hydrogen Peroxide Is Coupled to Biotic Defense Responses by ISOCHORISMATE SYNTHASE1 in a Daylength-Related Manner      

Abstract

While it is well established that reactive oxygen species can induce cell death, intracellularly generated oxidative stress does not induce lesions in the Arabidopsis (Arabidopsis thaliana) photorespiratory mutant cat2 when plants are grown in short days (SD). One interpretation of this observation is that a function necessary to couple peroxisomal hydrogen peroxide (H 2 O 2 )-triggered oxidative stress to cell death is only operative in long days (LD). Like lesion formation, pathogenesis-related genes and camalexin were only induced in cat2 in LD, despite less severe intracellular redox perturbation compared with SD. Lesion formation triggered by peroxisomal H 2 O 2 was modified by introducing secondary mutations into the cat2 background and was completely absent in cat2 sid2 double mutants, in which ISOCHORISMATE SYNTHASE1 (ICS1) activity is defective. In addition to H 2 O 2 -induced salicylic acid (SA) accumulation, the sid2 mutation in ICS1 abolished a range of LD-dependent pathogen responses in cat2, while supplementation of cat2 with SA in SD activated these responses. Nontargeted transcript and metabolite profiling identified clusters of genes and small molecules associated with the daylength-dependent ICS1-mediated relay of H 2 O 2 signaling. The effect of oxidative stress in cat2 on resistance to biotic challenge was dependent on both growth daylength and ICS1. We conclude that (1) lesions induced by intracellular oxidative stress originating in the peroxisomes can be genetically reverted; (2) the isochorismate pathway of SA synthesis couples intracellular oxidative stress to cell death and associated disease resistance responses; and (3) camalexin accumulation was strictly dependent on the simultaneous presence of both H 2 O 2 and SA signals.

The Heat Shock Factor A4A Confers Salt Tolerance and Is Regulated by Oxidative Stress and the Mitogen-Activated Protein Kinases MPK3 and MPK6

“…By contrast, expression of HSFA4A is inhibited by mutations that disrupt salicylic acid biosynthesis and salicylic acid-related pathogen defense (e.g. salicylic acid induction deficient2 phytoalexin deficient4 nonexpresser of PR1 genes1 and enhanced disease susceptibility1 Chaouch et al, 2010;Straus et al, 2010).…”

Cytosolic and Chloroplastic DHARs Cooperate in Oxidative Stress-Driven Activation of the Salicylic Acid Pathway

“…This might explain why DHAR2 can contribute to glutathione oxidation in vivo even though the associated DHAR activity, measured in vitro, appears to be negligible. Loss of CAT2 function induces SA accumulation in the absence of pathogens and associated pathogenesisrelated responses, including resistance to bacteria (Chaouch et al, 2010(Chaouch et al, , 2012. The induction of these responses is influenced by glutathione status (Mhamdi et al, 2010a;Han et al, 2013a).…”

“…Oxidized and reduced forms of glutathione and ascorbate were measured by plate-reader assay as described by Queval and Noctor (2007). Total SA was measured according to the protocol of Chaouch et al (2010).…”

Glutathione-dependent phytohormone responses

“…10,12 The cad2 and allelic mutations produce an effective block over the H 2 O 2 -triggered accumulation of GSSG that otherwise occurs in cat2 (Fig. 1B).…”