The Arabidopsis-accelerated cell death gene ACD2 encodes red chlorophyll catabolite reductase and suppresses the spread of disease symptoms

Accelerated cell death 2 (acd2) mutants of Arabidopsis have spontaneous spr eading cell death lesions and constitutive activation of defenses in the ab sence of pathogen infection. Lesion formation in acd2 plants can be trigger ed by the bacterial toxin coronatine through a light-dependent process. Cor onatine-triggered and spontaneous lesion spreading in acd2 plants also requ ires protein translation, indicating that cell death occurs by an active pr ocess. We have cloned the ACD2 gene; its predicted product shows significan t and extensive similarity to red chlorophyll catabolite reductase, which c atalyzes one step in the breakdown of the porphyrin component of chlorophyl l [Wuthrich, K. L., Bovet, L., Hunziger, P. E., Donnison, I. S. & Hortenste iner, S. (2000) Plant J. 21, 189-198]. Consistent with this, ACD2 protein c ontains a predicted chloroplast transit peptide, is processed in vivo, and purifies with the chloroplast fraction in subcellular fractionation experim ents. At some stages of development, ACD2 protein also purifies with the mi tochondrial fraction. We hypothesize that cell death in acd2 plants is caus ed by the accumulation of chlorophyll breakdown products. Such catabolites might be specific triggers for cell death or they might induce cellular dam age through their ability to absorb light and emit electrons that generate free radicals. In response to infection by Pseudomonas syringae, transgenic plants expressing excess ACD2 protein show reduced disease symptoms but no t reduced growth of bacteria. Thus, breakdown products of chlorophyll may a ct to amplify the symptoms of disease, including cell death and yellowing. We suggest that economically important plants overexpressing ACD2 might als o show increased tolerance to pathogens and might be useful for increasing crop yields.