To survive in a changing environment plants constantly monitor their surroundings. In response to several stresses and during photorespiration plants use reactive oxygen species as signaling molecules. The Arabidopsis thaliana catalase2 (cat2) mutant lacks a peroxisomal catalase and under photorespiratory conditions accumulates H2O2, which leads to activation of cell death. A cat2 double mutant collection was generated through crossing and scored for cell death in different assays. Selected double mutants were further analyzed for photosynthetic performance and H2O2 accumulation. We used a targeted mutant analysis with more than 50 cat2 double mutants to investigate the role of stress hormones and other defense regulators in H2O2-mediated cell death. Several transcription factors (AS1, MYB30, MYC2, WRKY70), cell death regulators (RCD1, DND1) and hormone regulators (AXR1, ERA1, SID2, EDS1, SGT1b) were essential for execution of cell death in cat2. Genetic loci required for cell death in cat2 was compared with regulators of cell death in spontaneous lesion mimic mutants and led to the identification of a core set of plant cell death regulators. Analysis of gene expression data from cat2 and plants undergoing cell death revealed similar gene expression profiles, further supporting the existence of a common program for regulation of plant cell death. Our results provide a genetic framework for further study on the role of H2O2 in regulation of cell death. The hormones salicylic acid, jasmonic acid and auxin, as well as their interaction, are crucial determinants of cell death regulation.

Plants are exposed to abiotic and biotic stress conditions throughout their lifespans that activates various defense programs. Programmed cell death (PCD) is an extreme defense strategy the plant uses to manage unfavorable environments as well as during developmentally induced senescence. Here we investigated the role of leaf age on the regulation of defense gene expression in Arabidopsis thaliana. Two lesion mimic mutants with misregulated cell death, catalase2 (cat2) and defense no death1 (dnd1) were used together with several double mutants to dissect signaling pathways regulating defense gene expression associated with cell death and leaf age. PCD marker genes showed leaf age dependent expression, with the highest expression in old leaves. The salicylic acid (SA) biosynthesis mutant salicylic acid induction deficient2 (sid2) had reduced expression of PCD marker genes in the cat2 sid2 double mutant demonstrating the importance of SA biosynthesis in regulation of defense gene expression. While the auxin- and jasmonic acid (JA)- insensitive auxin resistant1 (axr1) double mutant cat2 axr1 also led to decreased expression of PCD markers; the expression of several marker genes for SA signaling (ISOCHORISMATE SYNTHASE 1, PR1 and PR2) were additionally decreased in cat2 axr1 compared to cat2. The reduced expression of these SA markers genes in cat2 axr1 implicates AXR1 as a regulator of SA signaling in addition to its known role in auxin and JA signaling. Overall, the current study reinforces the important role of SA signaling in regulation of leaf age-related transcript signatures.

Ozone (O₃) entry into plant leaves depends on atmospheric O₃ concentration, exposure time and openness of stomata. O₃ negatively impacts photosynthesis rate (A) and might induce the release of reactive volatile organic compounds (VOCs) that can quench O₃, and thereby partly ameliorate O₃ stress. Water stress reduces stomatal conductance (g_s) and O₃ uptake and can affect VOC release and O₃ quenching by VOC, but the interactive effects of O₃ exposure and water stress, as possibly mediated by VOC, are poorly understood. Well-watered (WW) and water-stressed (WS) Brassica nigra plants were exposed to 250 and 550 ppb O₃ for 1 h, and O₃ uptake rates, photosynthetic characteristics and VOC emissions were measured through 22 h recovery. The highest O₃ uptake was observed in WW plants exposed to 550 ppb O₃ with the greatest reduction and poorest recovery of g_s and A, and elicitation of lipoxygenase (LOX) pathway volatiles 10 min–1.5 h after exposure indicating cellular damage. Ozone uptake was similar in 250 ppb WW and 550 ppb WS plants and, in both treatments, O₃-dependent reduction in photosynthetic characteristics was moderate and fully reversible, and VOC emissions were little affected. Water stress alone did not affect the total amount and composition of VOC emissions. The results indicate that drought ameliorated O₃ stress by reducing O₃ uptake through stomatal closure and the two stresses operated in an antagonistic manner in B. nigra.