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

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

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Greenberg, J. T. Hoogstraten, R. Mach, J. M. Castillo, A. R.
Description	Author Affiliation: Mach JM ( Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL 60637, USA.);
Abstract	accelerated cell death 2 (acd2) mutants of Arabidopsis have spontaneous spreading cell death lesions and constitutive activation of defenses in the absence of pathogen infection. Lesion formation in acd2 plants can be triggered by the bacterial toxin coronatine through a light-dependent process. Coronatine-triggered and spontaneous lesion spreading in acd2 plants also requires protein translation, indicating that cell death occurs by an active process. We have cloned the ACD2 gene; its predicted product shows significant and extensive similarity to red chlorophyll catabolite reductase, which catalyzes one step in the breakdown of the porphyrin component of chlorophyll [Wüthrich, K. L., Bovet, L., Hunziger, P. E., Donnison, I. S. & Hörtensteiner, S. (2000) Plant J. 21, 189-198]. Consistent with this, ACD2 protein contains a predicted chloroplast transit peptide, is processed in vivo, and purifies with the chloroplast fraction in subcellular fractionation experiments. At some stages of development, ACD2 protein also purifies with the mitochondrial fraction. We hypothesize that cell death in acd2 plants is caused by the accumulation of chlorophyll breakdown products. Such catabolites might be specific triggers for cell death or they might induce cellular damage 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 not reduced growth of bacteria. Thus, breakdown products of chlorophyll may act to amplify the symptoms of disease, including cell death and yellowing. We suggest that economically important plants overexpressing ACD2 might also show increased tolerance to pathogens and might be useful for increasing crop yields.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	2
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Arabidopsis Proteins Arabidopsis Genetics Genes, Plant Oxidoreductases Plant Diseases Plant Proteins Alleles Amino Acids Toxicity Apoptosis Regulatory Proteins Enzymology Microbiology Radiation Effects Cell Death Chlorophyll Metabolism Chloroplasts Cloning, Molecular Cycloheximide Pharmacology DNA, Antisense DNA, Complementary Immunity, Innate Indenes Mitochondria Molecular Sequence Data Phenotype Drug Effects Plants, Genetically Modified Protein Biosynthesis Protein Synthesis Inhibitors Pseudomonas Pathogenicity Reactive Oxygen Species Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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