ArabidopsisACCELERATED CELL DEATH2 Modulates Programmed Cell Death

Abstract

The Arabidopsis thaliana chloroplast protein ACCELERATED CELL DEATH2 (ACD2) modulates the amount of programmed cell death (PCD) triggered by Pseudomonas syringae and protoporphyrin IX (PPIX) treatment. In vitro, ACD2 can reduce red chlorophyll catabolite, a chlorophyll derivative. We find that ACD2 shields root protoplasts that lack chlorophyll from lightand PPIX-induced PCD. Thus, chlorophyll catabolism is not obligatory for ACD2 anti-PCD function. Upon P. syringae infection, ACD2 levels and localization change in cells undergoing PCD and in their close neighbors. Thus, ACD2 shifts from being largely in chloroplasts to partitioning to chloroplasts, mitochondria, and, to a small extent, cytosol. ACD2 protects cells from PCD that requires the early mitochondrial oxidative burst. Later, the chloroplasts of dying cells generate NO, which only slightly affects cell viability. Finally, the mitochondria in dying cells have dramatically altered movements and cellular distribution. Overproduction of both ACD2 (localized to mitochondria and chloroplasts) and ascorbate peroxidase (localized to chloroplasts) greatly reduces P. syringae-induced PCD, suggesting a pro-PCD role for mitochondrial and chloroplast events. During infection, ACD2 may bind to and/or reduce PCD-inducing porphyrin-related molecules in mitochondria and possibly chloroplasts that generate reactive oxygen species, cause altered organelle behavior, and activate a cascade of PCD-inducing events.

The Arabidopsis Spontaneous Cell Death1 gene, encoding a ζ-carotene desaturase essential for carotenoid biosynthesis, is involved in chloroplast development, photoprotection and retrograde signalling

“…It is interesting to notice that spc1-1 has a lower level of chlorophylls a and b, which appears to be correlated to the reduced expression of PORB and CAO. The impaired chlorophyll metabolism and abnormal chloroplast development have been attributed as an important mechanism to trigger spontaneous cell death in a number of mutants, including Arabidopsis-accelerated cell death2 (acd2) [63,64], acd1 [65][66][67] and maize lethal leaf spot-1 (lls1) [68,69]. ACD1 and LLS1 are believed to be ortholog genes in Arabidopsis and maize [65,66,69].…”

“…ACD1 and LLS1 are believed to be ortholog genes in Arabidopsis and maize [65,66,69]. These three genes, all encoding key enzymes for chlorophyll degradation, presumably function to prevent the formation of ROS or free radicals generated from photooxidation, thereby negatively regulating cell death [63,64,69]. In spc1, however, the reduced chlorophyll level may not be a direct casual factor for the cell death phenotype, since spc1 and other three mutations (acd1, acd2 and lls1) appear to involve different Although most plastid proteins are encoded by nuclear genes, plastid-derived signals, however, can also regulate expression of nuclear genes encoding plastid-localized proteins.…”

Arabidopsis AZI1 family proteins mediate signal mobilization for systemic defence priming

“…Moreover, during SAR-inducing infections AZA levels increase 10,12,32 , probably due to an increase of nitric oxide/reactive oxygen species in chloroplasts 31,46 . AZI1, EARLI1 and AZI3 are upregulated by AZA and/or conditions that promote nonenzymatic lipid peroxidation 47 .…”

Update on the biochemistry of chlorophyll breakdown

“…Cell death is lightdependent and coincides with the production of singlet oxygen (Pattanayak et al 2012). However, the fact that cell death in acd2 also occurred in Chl-free root protoplasts, called into question the role of RCCR/ACD2 as a Chl catabolic enzyme (Yao and Greenberg 2006). Complementation of acd2 with AtRCCR enzymes that exhibited different C1-stereospecificities as outlined above, resulted in corresponding stereospecifically uniform patterns of catabolites (Pružinská et al 2007).…”

“…RCCR was experimentally shown to localize to the chloroplast (Wüthrich et al 2000), but it also partially localizes to mitochondria, particularly upon stresses, such as pathogen infection or protoporphyrin IX treatment (Yao and Greenberg 2006). In addition, cell death in acd2 involves an early mitochondrial oxidative burst (Yao et al 2004).…”