LESION SIMULATING DISEASE 1 Is Required for Acclimation to Conditions That Promote Excess Excitation Energy    

Abstract

The lsd1 mutant of Arabidopsis fails to limit the boundaries of hypersensitive cell death response during avirulent pathogen infection and initiates unchecked lesions in long day photoperiod giving rise to the runaway cell death (rcd) phenotype. We link here the initiation and propagation of rcd to the activity of photosystem II, stomatal conductance and ultimately to photorespiratory H 2 O 2 . A cross of lsd1 with the chlorophyll a/b binding harvesting-organelle specific (designated cao) mutant, which has a reduced photosystem II antenna, led to reduced lesion formation in the lsd1/cao double mutant. This lsd1 mutant also had reduced stomatal conductance and catalase activity in short-day permissive conditions and induced H 2 O 2 accumulation followed by rcd when stomatal gas exchange was further impeded. All of these traits depended on the defense regulators EDS1 and PAD4. Furthermore, nonphotorespiratory conditions retarded propagation of lesions in lsd1. These data suggest that lsd1 failed to acclimate to light conditions that promote excess excitation energy (EEE) and that LSD1 function was required for optimal catalase activity. Through this regulation LSD1 can influence the effectiveness of photorespiration in dissipating EEE and consequently may be a key determinant of acclimatory processes. Salicylic acid, which induces stomatal closure, inhibits catalase activity and triggers the rcd phenotype in lsd1, also impaired acclimation of wild-type plants to conditions that promote EEE. We propose that the roles of LSD1 in light acclimation and in restricting pathogen-induced cell death are functionally linked.

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

“…Particularly in the leaves of C 3 plants, these organelles can be a rich source of H 2 O 2 through the photorespiratory glycolate oxidase reaction (Noctor et al, 2002). A role for peroxisomal H 2 O 2 in pathogen responses is consistent with studies of mutants for Ser:glyoxylate aminotransferase (Taler et al, 2004), an enzyme immediately downstream of glycolate oxidase in the photorespiratory pathway, as well as effects of photorespiratory conditions on the phenotypes of the lsd1 mutant (Mateo et al, 2004). Given the high catalase activities of wild-type plants, it is likely that this enzyme must be down-regulated to allow H 2 O 2 produced in leaf peroxisomes to contribute to signaling during a biotic challenge (Foyer et al, 2009).…”

Early Senescence and Cell Death in Arabidopsis saul1 Mutants Involves the PAD4-Dependent Salicylic Acid Pathway

“…It has been shown that PAD4 and EDS1 participate not only in resistance to pathogens but also in the transduction of photooxidative stress signals resulting in cell death and growth inhibition. Cell death and growth inhibition phenotypes of lsd1, acd6-1, cpr1, and cpr6 mutants require the presence of PAD4 and EDS1, as demonstrated by the rescue of mutant phenotypes in double mutants with pad4 or eds1 (Jirage et al, 2001;Rustérucci et al, 2001;Mateo et al, 2004;Ochsenbein et al, 2006;Mühlenbock et al, 2008;Ng et al, 2011). The SA amplification loop is also crucial for cell death and senescence, increased SA content, and gene expression changes in saul1 mutants challenged by low light (Fig.…”

Oxidative Stress: Antagonistic Signaling for Acclimation or Cell Death?

“…SA is involved in this response and may be linked to increased production of glutathione, thus enhancing cellular antioxidant capacity (Mou et al, 2003;Mateo et al, 2006). However, a second regulatory protein, LESION-SIMULATING DISEASE1 (LSD1), also prevents lesion spread and enhances ROS-scavenging capacity by increasing superoxide dismutase and catalase activities (Kliebenstein et al, 1999;Mateo et al, 2004). In cells neighboring the lesion, an alternative EDS1-based antagonistic system between pro-death and anti-death pathways is established.…”